Edward C. Covington, MD and Margaret M. Kotz, DO
CHAPTER OUTLINE
■ INTRODUCTION
■ PSYCHOLOGICAL MODULATION OF PAIN
■ SOMATOFORM DISORDERS/SOMATIC SYMPTOM DISORDERS
■ THE ROLE OF THE ENVIRONMENT
■ DEVELOPMENTAL ISSUES
■ IDENTIFYING PSYCHOLOGICAL CONTRIBUTIONS TO PAIN
■ PSYCHOLOGICAL APPROACHES TO THE TREATMENT OF PAIN
■ CONCLUSIONS
INTRODUCTION
This chapter addresses primarily chronic, nonmalignant pain; however, many of the principles discussed may be applicable in acute, malignant, and recurrent acute pain as well. Although the focus is on psychological interventions, such interventions are most effective when combined with rehabilitation techniques, appropriate pharmacotherapy, and interventions. The focus on psychological issues that should be addressed tends to imply incorrectly that the psyche typically exacerbates the condition of those with chronic pain, when in fact most people with chronic pain have coping mechanisms that enable them to continue to function productively and enjoy life. Ultimately, few of us fully escape protracted pain, and the psyche is often the facility that enables us to remain fulfilled and productive.
This volume comes after more than four decades of intensive investigations into the neurobiology of pain and into surgical, interventional, pharmacologic, and psychological treatments for it. We have seen major medical advances and considerable improvements in industrial and highway safety, yet it seems that more people are disabled with pain now than ever before. In the case of chronic low back pain (LBP), the leading pain-related cause of work disability, we are devoting more resources to its diagnosis and treatment, yet apparently have worse functional outcomes (1–3). Between 1971 and 1981, the number of people with disabling back problems increased 168%, while the population increased only 12.5% (4). In 1997, 20.7% of those with back pain reported limitations in physical function, a figure that rose to 24.7% in 2005 (1). This seeming paradox may result in part from our failure to adequately address the psychological side of chronic pain. That is to say, it is likely that much of the suffering and disability that persist despite treatment of chronic noncancer pain (CNCP) results from the focus of our health care system on the pathology rather than the person. This is in the face of compelling evidence that psychosocial variables predict onset, chronicity, and outcomes in back pain more than do somatic variables. These influences frequently override tissue destruction in determining the experience of the person who has pain.
In a 4-year prospective study of 3,020 aircraft workers, job dissatisfaction and poor performance appraisals strongly predicted reports of acute back pain at work (5). Subjects who “hardly ever” enjoyed their jobs were more than twice as likely to report a back injury as those who “almost always” enjoyed their work. Another prospective study of 1,412 pain-free employees confirmed that those dissatisfied with their work were twice as likely to seek care for LBP during a 12-month period as those who were satisfied, while those who felt underpaid were nearly four times as likely, and those in the lowest socioeconomic stratum were almost five times as likely to seek care for LBP (6). Subsequent investigations have confirmed that the first report of a back injury at work is independently predicted by prior LBP, physical work stress, and psychological intolerance of the job.
This chapter summarizes the psychological factors that have a major influence on pain and pain-associated functional impairment and then outlines treatments that have been shown to be beneficial. However, it should be recognized that good clinical care may be necessary but not sufficient to end what could be considered an epidemic of disability related to pain, since systemic and societal variables also need to be addressed in the aggregate at policy levels.
Clinical practice would be easier if we could dichotomize the factors that modulate pain and dysfunction into organic versus psychological and concepts of “mind–body dualism” linger in our literature and thinking. Indeed, it is helpful when considering interventions to attempt to discern the extent to which malfunctions result from “hardware failures” and the extent to which they are due to “software errors.” However, it seems that the closer we examine our patients, the murkier is this distinction, so that each attempt to classify a phenomenon as purely psychological or organic introduces error. The lesson is that we ignore either at the risk of compromising our understanding.
Accumulating evidence supports the hypothesis that the linguistic connections we make between social pain and physical pain are more than metaphorical. Being “broken hearted” or having “hurt feelings” may reflect a neurologic reality. It was once common in the rural South to hear patients refer to pain as “a misery in my back.” This seems to capture the essence of chronic pain—it is a misery. Eisenberger et al. (7) showed that the brain activation (anterior cingulate gyrus, ventral prefrontal cortex) following experimental social exclusion was similar to that seen in experimental physical pain. Subsequently they showed that social distress increased pain sensitivity and that pain sensitivity predicted sensitivity to rejection (8). Studies such as these, and others mentioned below, seem to render many of the organic versus functional arguments moot.
The biopsychosocial model as described by Birket-Smith (9) (Fig. 94-1) is appropriate for all but the most short-lived painful conditions. (In truth, all pain is modulated by psychological and environmental factors; however, they can often be ignored in such situations as the acute treatment of fractures, appendicitis, and similar conditions.) In this chapter, a number of psychological factors will be discussed that have been shown to impact pain, pain-related suffering, and functional impairment. Although they are presented separately for ease of conceptualization, they are interacting and overlapping in their effects.
FIGURE 94-1 The biopsychosocial model as described by Birket-Smith. (From Birket-Smith M. Somatization and chronic pain. Acta Anaesthesiol Scand 2001;45:1114–1120.)
PSYCHOLOGICAL MODULATION OF PAIN
Does the Psyche Cause Pain?
Patients with pain who have not been provided with an explanatory medical diagnosis often feel discounted, feel disparaged, and made to feel that “the pain is only in my head.” And in fact, historically, the inability to explain symptoms medically has led clinicians either to doubt the reality of the symptoms or to assume that they were psychologically caused. As will be demonstrated below, while beliefs, fears, expectations, and affects both amplify and mitigate pain perception, this is quite different from stating that they cause it (see Ref. (10)).
While the concept of “medically unexplained symptoms” was central to the diagnosis of somatoform disorders in Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV), the concept has now been removed from the DSM-5. This seems a fortunate change, since failure to find a medical explanation can never demonstrate that there is none. Acute experimental pain can be created with suggestion, beliefs, and expectations; however, demonstrations of this occur in the laboratory, and its relevance to clinical chronic pain is unclear.
Pain is primarily a function of the nervous system and, especially in the case of protracted and/or neuropathic pain, may bear little relation to the intensity of peripheral stimulation. The classical picture of pain as a signal transmitted from the receptor to the cortex is a misrepresentation, since such processes as sensitization, descending inhibition and facilitation of pain, and neuroplastic changes fully account for several previously idiopathic conditions (11–13).
Coghill et al. (14) applied a 49°C thermode to the forearms of healthy volunteers, who rated the resulting pain. Ratings varied from 1/10 to 9/10. Those who reported higher levels of pain showed more activation on functional magnetic resonance imaging (fMRI) in the anterior cingulate, somatosensory cortex, and prefrontal cortex. The conclusion was that those reporting more pain do indeed have more pain (absent incentives to misreport).
Selective breeding produces strains of rats that are extremely vulnerable to the development of neuropathic pain after sciatic nerve ligation and other strains that are virtually immune to it (15). Multiple genetic variations have been identified in humans that modify pain perception or opioid responsivity (16). It is thus compellingly established that unexplained pain is not necessarily psychogenic and that variations in pain perception may result from genetic factors. Therefore, clinicians should be reluctant to invoke psychosocial explanations for pain solely because it seems inappropriate or excessive.
Emotional Distress
Chronic pain is often associated with emotional symptoms that may not meet criteria for a psychiatric diagnosis but nevertheless contribute substantially to suffering and require treatment. Emotions modulate pain perception acutely, predict its persistence, and impact treatment response. Berna et al. (17) found that experimentally induced negative (sad) mood states in healthy volunteers led to increased unpleasantness of experimental pain. Imaging with fMRI demonstrated that this was associated with increased activity in the prefrontal cortex, anterior cingulate, and hippocampus. Those with the largest increase in pain unpleasantness showed the greatest activation of the inferior frontal gyrus and amygdala. Previous investigators had demonstrated that experimental pain perception was modified by induction of happy or sad moods by short stories, hypnotic induction, and other methods (18,19). Notably, these changes are not contingent on the person’s meeting criteria for a psychiatric diagnosis of depression or anxiety, but only on the presence of the mood state.
Bair et al. (20) reviewed studies (including their own) of chronic pain patients that found a 30% to 60% co-occurrence of depression (variously defined), a 35% prevalence of anxiety (including DSM-III-R–based generalized anxiety disorder, panic disorder, simple phobia, social phobia, and agoraphobia), and many with all three—pain, depression, and anxiety (21). In the authors’ study of 500 patients with chronic musculoskeletal pain, 20% had comorbid depression, 3% comorbid anxiety, and 23% comorbid depression and anxiety. Variations in rates often reflect differences in settings, methodology, and criteria, as well as diagnostic ambiguity resulting from the overlap of affective symptoms with those of pain. For example, insomnia from pain and drugs, loss of energy from deconditioning, and guilt from having become a burden can mimic symptoms of mood disorder.
A clinical population tends to select for those with depression; however, Miller and Cano (22) used computer-assisted telephone interviewing to obtain a representative community sample in the state of Michigan (n = 1,179). The prevalence of chronic pain was 21.9%, approximately 35% of whom had comorbid depression. In a telephone survey of nearly 19,000 Europeans, Ohayon and Shatzberg (23) found that 75% of those with chronic pain had at least one core depressive symptom. While depression in this group is commonly attributed to pain, other factors, such as restricted activities and a sense of helplessness, may be equally important (24).
Anxiety has long been associated with pain. In a representative sample of 3,032 US adults, those with arthritis, migraine, and back pain were markedly more likely to have depression (odds ratio [OR] 1.48 to 2.84) but even more so to have an anxiety disorder (OR 2.09 to 3.86) (25). Recently, a random sample of citizens of Heidelberg, Germany, with chronic back pain was interviewed with use of the SCID-I + II. Of these, 20.9% had an anxiety disorder and 12.7% a mood disorder (26). Anxiety not only compounds the suffering in CNCP, it also impedes treatment. Baseline anxiety, as well as depression, predicted functional and symptomatic outcome in sciatica (27). In a group of veterans seeking treatment for posttraumatic stress disorder (PTSD), Shipherd et al. found that 66% had chronic pain as well (28).
A specific anxiety disorder, PTSD, is highly associated with pain (see review (29)). Defrin et al. found that, compared to healthy controls and those with anxiety disorders, patients with PTSD had higher rates of chronic pain, more intense pain, and pain in more body regions. Thresholds to experimental pain were higher than the control groups; however, when the thresholds were exceeded, patients experienced the pain as much more intense (30).
Based on structured interviews using the SCID, Knaster et al. (31) found that 37% of patients attending a university-affiliated pain center in Helsinki met diagnostic criteria for major depression, 25% for anxiety disorders, and 12% for substance use disorder. (They excluded patients taking “strong opioids.”) The majority of anxiety disorders preceded pain, while most depressive disorders followed it. Somatoform disorders were not assessed. The lifetime prevalence of any psychiatric disorder was 75%, and the current prevalence of depression was seven times those found in a comparison Finnish community sample and six times higher than those found for anxiety.
In recent years, the phenomenon of “anxiety sensitivity” has been found to play a role in pain. The term refers to an abnormal fear of the normal sensations associated with anxiety. Anxiety sensitivity amplifies experimental pain and is associated with muscular, abdominal, and head pain, as well as with impaired coping (32,33).
There has been debate as to whether pain leads to depression or vice versa. In fact, each has been shown to predict the future development of the other (34), and each diminishes successful treatment of the other (35,36).
Research into the factors that predict so-called “chronification,” the transformation of acute to chronic pain, has also implicated depression. Shaw et al. (37) studied 140 men with first-onset LBP of approximately 8 weeks’ duration. Chronification was predicted by lifetime history of depression (OR 4.99), lifetime generalized anxiety disorder (GAD) (OR 2.45), posttraumatic stress (OR 3.23), and nicotine dependence (OR 2.49). Wylde et al. (38) studied persistent postoperative pain in patients having total joint replacement (632 knee and 662 hip). Persistent postoperative pain was reported by 44% of TKR patients and 27% of THR patients. In 15% of TKR patients and 6% of THR patients, the pain was severe or extreme. Although depression was found to predict persistent pain (OR 1.27 and 1.29, respectively), the presence of multiple pain problems was dramatically more influential. Those with 3 to 4 pain problems had odds ratios of 7.02 and 8.45, while those with ≥5 pain problems had ratios of 14.8 and 11.78.
Maletic and Raison reviewed evidence supporting a biologic relationship between depression, fibromyalgia, and neuropathic pain. These conditions may share genetic vulnerabilities and overlapping neurochemistry and can be triggered or modulated by environmental stressors (39). Additional light has recently been shed on this relationship by Kim et al. who found that that brain indoleamine 2,3-dioxygenase 1 (IDO1), a rate-limiting enzyme in tryptophan metabolism, plays a key role. Rats in which chronic pain was produced by inflammatory arthritis developed both depressive behavior and IDO1 upregulation in the hippocampus. In humans, they found elevated plasma IDO activity in patients with both pain and depression, and in rats, this was found after induction of “anhedonia” by chronic social stress. IDO1 gene knockout or pharmacologic inhibition of hippocampal IDO1 attenuated both nociceptive and depressive behavior (40).
In summary, we can conclude the following:
■ Mood disturbance can elicit pain.
■ Pain can elicit mood disturbance.
■ Either can exacerbate the other.
■ Either can make the other treatment resistant.
■ Depression predicts chronification of acute pain.
■ Depression and pain likely share some neurochemical abnormalities.
While anxiety and depression have been extensively studied in those with pain, there is no corresponding “anger disorder” (41), yet anger is a major cause of suffering in these patients. Trost et al. (42) reviewed the role of anger in chronic pain and the cognitive processes that contribute to it. Anger increases pain-related suffering and interferes with life activities, while it reduces response to treatment (43,44). Forgiveness, in contrast, seems therapeutic (45). Cognitive dimensions of anger include frustration, blame (v.i.), and perceived injustice. Patients are frustrated in their efforts to carry out life functions, to achieve a cure, and to garner needed support. There is often a sense of betrayal as those who “should have” taken care of them (employers, health care providers) failed to do so.
Gratitude may be considered the converse of anger and resentment, and a growing body of evidence points to associations between gratitude and both psychological and physical health (46) as well as resilience following natural disasters (47). In adolescents, gratitude was associated not only with mental well-being but also with a lower prevalence of physical symptoms, an effect that appeared mediated by satisfaction with relationships (48). In a sample of 224 patients with chronic pain, Ng and Wong (49) found gratitude to be associated with increased sleep and fewer symptoms of depression and anxiety.
Attention and Vigilance
All perceptions, including pain, are amplified when attended to and are attenuated by distraction. The neurobiologic basis of these effects is under active investigation, and Legrain et al. (50) have reviewed top-down (corticofugal) and bottom-up (corticopetal) influences on the attention elicited by a painful stimulus. Experience deceives us, as it seems that “paying attention” is purely a matter of directing our consciousness; however, attention has been shown to modify pain transmission at the level of the spinal cord dorsal horn. This results from the influence of descending inhibitory and facilitatory pathways regulated by the nucleus raphe magnus (51), which is, in turn, under the influence of descending fibers from the amygdala (52). Bushnell et al. (53) found that distraction from a painful stimulus diminished both pain report and activation of the primary somatosensory cortex. Sprenger et al. (54) used high-resolution fMRI to show that a distracting memory task inhibited afferent signals of thermal pain at the level of the dorsal horn, and Petrovic et al. (55) showed that a maze task reduced the experience of pain and activity in the somatosensory association areas and periaqueductal gray/ midbrain (as reflected in the PET scan) in subjects given the cold pressor test. It appears that the memory task activated descending inhibitory pathways that attenuated pain signals at their point of entry.
People may respond to chronic pain by retreating to the bedroom, isolating socially, and limiting stimulation, all in an effort to feel better. These behaviors may so limit competing stimulation that pain becomes all consuming, which has led to the expression, “If life is empty, pain will fill it up.”
Expectations
Expectations are important in two ways: They impact both pain perception and recovery outcome. Iles et al. (56) reviewed studies demonstrating that patient expectations of recovery predict return to work in subacute LBP. Clay et al. (57) confirmed that low recovery expectations predicted pain-related work disability. In a study of acupuncture and massage for LBP, Kalauokalani et al. (58) found that patient expectations correlated with response to each treatment and with which treatment produced better results. These studies are unable to discern whether patients are simply accurate predictors or whether low expectations impede recovery. Suggesting that expectations change perception, Koyama et al. (59) showed that raising and lowering expectations of experimental pain produced concordant changes in both pain report and activation of thalamus, insula, prefrontal cortex, anterior cingulate cortex, and other brain regions. Sawamoto et al. (60) created the expectation of pain with a series of painful thermal stimulations and then administered a comfortably warm stimulation. When a painful stimulus was expected, there was activation of the nucleus accumbens and posterior insula in response to the neutral stimulus, as reflected in fMRI. There was also an increase in the perceived unpleasantness of the stimulation. In summary, it is clear that expectations can increase or decrease the perception of pain and the response to pain treatment.
Fear and Deconditioning
The profound impairment that results from prolonged inactivity often begins with a fear of injury. A vicious cycle begins in which inordinate fear leads to inactivity, which in turn leads to deconditioning and a state of increased fragility as loss of strength and range of motion increase susceptibility to strains and sprains (61). The fear-avoidance model of chronic pain suggests that conditioned responses develop following situations or behaviors associated with pain, such that these situations acquire the capacity to elicit pain on a learned basis, and therefore their avoidance is reinforcing (62). Later studies indicate that this conditioning can occur without the direct experience of increased pain, in response to verbal communication (“That could paralyze you.”) or witnessing others experience pain. Fear of injury is compounded by the individual’s belief that he is ill or fragile. Kori et al. (63) coined the term kinesophobia to denote an irrational fear that movement or activity will lead to reinjury. Pain-related fear predicts functional impairment better than does pain severity alone (64,65). It interferes with patients’ efforts to focus away from pain onto tasks and other things (66). Inordinate fear may at times be iatrogenic (67), and it is distressingly common to hear patients report such physician statements as “You have the back of an 80-year-old,” and “You don’t need surgery now but you will,” and “This is the worst case of _____ we’ve ever seen.”
In chronic pain, information is therapy. We have been surprised and gratified by patients’ (and families’) responses to a 40-minute video that summarizes the neurobiology of pain in lay terms. They found it reassuring and freeing to learn that the perception of even severe pain could be “real,” without implying a bleak prognosis or a need for self-protection.
Cognitions and Coping
The role of cognition in psychiatric conditions has been recognized for over 35 years (68–70), and this understanding has expanded to include chronic pain. The underlying premise of cognitive theories is that individuals react to their interpretation and understanding of events, rather than to the events themselves. The terminal cancer patient who is convinced that “the surgeon got it all” will be more content than the healthy patient with hypochondriasis who fears occult pathology. Beliefs such as “These exercises must be tearing something loose,” “I will resume social activities after I am well,” and “I can’t go out if I am in pain” have obvious effects on adaptation. Maladaptive cognitions have the quality of being automatic and habitual, so that they rarely are examined for validity. They are accepted by the patient, even when clearly illogical to others.
The Implications of Pain
Cognitive factors affect pain in several ways (71,72). The aversive quality of pain is modified by its interpretation (73,74), so that it is more distressing if thought to presage bodily harm. The best studied example of maladaptive cognition is catastrophic thinking, a trait associated with poor pain tolerance and coping (75). “Catastrophizing” describes the automatic interpretation of events in the worst way possible: if a spouse is late returning home, there “must have” been an accident. In the case of chronic pain, such catastrophic interpretations as “The nerves are being crushed,” or “I may become paralyzed,” increase dysfunction, worsen pain, and hinder coping (76,77). Negative thoughts that reduce pain tolerance include those emphasizing the aversiveness of the situation, the inadequacy of the person to bear it, or the physical harm that could occur (72). Jensen et al. (78) reviewed studies of the effects of cognitive and coping factors in patients with such disabilities as multiple sclerosis, muscular dystrophy, and spinal cord injury and found them to be relevant to these populations as well.
Providers can reduce suffering and improve function by (a) validating the patient’s complaint, (b) describing the biology of the pain in terms that emphasize neurologic sensitization and minimize peripheral pathology, and (c) providing clear guidance as to which activities the patient can safely perform—even if they are painful.
Helplessness versus Self-Efficacy
Cognitive influences include not only beliefs regarding pain but also those regarding the person experiencing it. One’s sense of personal power and competence modify coping (79). Seligman’s (80) model of learned helplessness in depression suggests that those who feel unable to control events in their lives will respond passively to them, become depressed, and experience increased disability and pain. Conversely, belief in self-efficacy is a major determinant of successful coping (81,82) and predicts better functioning in fibromyalgia and arthritis (83,84). These beliefs are favor-ably associated not only with pain and function but also with treatment outcomes. Costa et al. (85) recently confirmed the association of self-efficacy with pain and function in chronic back pain and fear of movement with the converse. They followed patients for a year and found that self-efficacy predicted improvements in pain and function much better than did fear of movement.
Locus of Control
Closely related to the concept of self-efficacy is that of locus of control (LOC), which has to do with attributions of causality. People differ in their tendency to perceive events as determined by their own choices and behavior (“internal LOC”) or by outside forces, such as family members and physicians (“powerful others”), or chance. In several studies, those with an internal LOC felt and functioned better (86), while those with a “chance/external” LOC reported depression and anxiety, felt helpless, and relied on maladaptive coping strategies (87). Hadjistavropoulos and Shymkiw (88) reviewed studies finding that internal LOC beliefs were associated with better rehabilitation outcomes, including continued use of exercises at follow-up, while those with external LOC beliefs were associated with fewer gains.
Not all studies have found this. For example, in a 2-year prospective study of workers with LBP, Richard et al. (89) found that self-efficacy predicted successful return to work, while health LOC did not. Oliveira et al. (90) found that patients in physical treatment had a less internal LOC than did those awaiting treatment, suggesting that providing patients with treatment may diminish their confidence in their own ability to improve pain and function.
Blame
The harboring of blame appears to be toxic to patients attempting to recover from injury. DeGood and Kiernan (91) found that chronic pain patients who blame others for their pain reported greater mood distress and behavioral disturbance, poorer response to past treatments, and lower expectation of future benefits. Clay et al. followed 168 patients with mostly mild to moderate orthopedic injuries (57). The odds of reporting pain at 6 months was 13.5 times greater in those who reported high initial pain and held external attributions of responsibility for their injury. Severity of injury was not a significant predictor of outcome. Significantly, those reporting work-related disability were 11 times more likely to have external attribution of responsibility. In addition to pain and disability, blame has been found to predict posttraumatic stress disorder following motor vehicle accidents (92,93) and recovery from traumatic brain injury (94).
SOMATOFORM DISORDERS/SOMATIC SYMPTOM DISORDERS
The diagnosis of somatoform disorders in the DSM-IV was predicated primarily on the presence of medically unexplained symptoms. This was quite problematic, since a number of pains that were previously “medically unexplained” and therefore thought to be “nonphysiologic” have now been explained by such processes as central sensitization, neuroplasticity, and glial activation. The category of “somatoform disorders” has now been eliminated, and the DSM-5 category of “somatic symptom disorders” will apply to many patients previously diagnosed with somatoform disorders (95,96). Whether the symptoms are medically explained is no longer a criterion for the diagnosis; instead, the emphasis is on distress, dysfunction, and disproportionate thoughts, feelings, and behaviors.
The ICD-10, however, continues to rely on the older concepts and defines “somatization” as “the repeated presentation of physical symptoms, together with persistent requests for medical investigations, in spite of repeated negative findings and reassurances by doctors that the symptoms have no physical basis (97).” “Somatization” alone is not a clinical diagnosis but rather a description of a process whereby a patient expresses psychological problems via less stigmatizing and typically more socially acceptable physical complaints.
The DSM-IV condition “pain disorder” was characterized by significant pain (causing distress or impairment) “that is judged to be psychologically caused, exacerbated, or perpetuated.” Criteria for making this judgment were not provided (98). This diagnosis has been eliminated, as has “somatization disorder,” which required a multitude of medically unexplained symptoms (four of them pain related). These have been replaced with “somatic symptom disorder,” which offers a specifier for “with predominant pain,” if applicable. These newer diagnoses may be easier to apply clinically. Somatic symptom disorder involves one or more somatic symptoms that are distressing or result in significant disruption of daily life. Excessive feelings, thoughts, or behaviors related to the somatic symptoms or associated health concerns are manifested by at least one of the following: disproportionate and persistent thoughts about the seriousness of one’s symptoms, persistently high level of anxiety about health symptoms, or excessive time and energy devoted to these symptoms or health concerns. Although any one somatic symptom may not be continuously present, the state of being symptomatic is persistent (typically more than 6 months) (99).
Pain complaints and pain-related disability are prominent in those who have somatic symptom disorders, that is, those who have inordinate distress or dysfunction and who have disproportionate thoughts, feelings, and behaviors related to their symptoms. Such people tend to seek a great deal of health care that can be toxic to them. It is thus worthwhile, if only to avoid potentially harmful studies and treatments, to determine the extent to which those complaints should be managed psychiatrically and behaviorally as opposed to eliciting multiple MRI scans, repeated courses of steroids, and palliative surgeries.
The need for a predominantly behavioral approach is suggested by nonneurologic findings on examination and behavioral inconsistencies. Patients may demonstrate behaviors that are incompatible with the degree of impairment they report. Some may be cheerful despite a distressing degree of disability, while others appear to suffer severely, cannot sleep, and demonstrate suicidality. This suggests that these conditions will eventually be shown to subsume different types of pathology. Patients may be unable to discuss nonsomatic issues. If questioned about family, work, sports, or politics, they may rapidly deviate to symptoms, doctors, tests, and treatments to a degree not typical even in those with severe medical illness.
The mechanisms by which psychological factors modify pain perception are complex and incompletely understood. Importantly, the symptoms are real; that is, the patients are not simply exaggerating. Given the growing evidence that people who report high levels of pain have concordant cortical activation in pain-relevant areas, and that reinforcing pain behavior seems to produce actual increases in pain perception, it is probable that painful symptoms that follow emotional trauma are physiologically based as well. Van der Kolk et al. (100) studied 520 subjects who had experienced significant trauma. PTSD, dissociation, somatization, and affect dysregulation were highly interrelated, and the authors concluded that these conditions represent a spectrum of responses to trauma. Scores suggested a hierarchy of toxicity, such that disaster victims were less affected than victims of adult interpersonal trauma, and those who experienced childhood trauma were most affected.
Chronic Pain Syndrome
Chronic pain syndrome (CPS) is a somewhat archaic term that is still often heard, perhaps because it is a useful concept. It must be distinguished from CNCP. The term was used to describe patients with inordinate impairment and behavioral abnormalities (101) and was defined as intractable pain of 6 months’ or more duration, accompanied by marked alterations of behavior, with depression or anxiety; marked restriction in daily activities; excessive use of medication and frequent use of medical services; no clear relationship to organic disorder; and history of multiple, nonproductive tests, treatments, and surgeries. Thus, CPS is predominantly a behavioral syndrome that affects a minority of patients with chronic pain. The term properly directs therapy toward the reversal of regression and away from an exclusive focus on nociception, but does not substitute for a careful diagnosis of the underlying physiologic, psychological, and conditioning components of the syndrome. Some of the controversy regarding chronic opioid analgesia may actually be an argument between those who have found opioids useful in treating chronic pain and those who have found them harmful in chronic pain syndrome. Patients with pain who have an active addictive disorder are probably at increased risk for chronic pain syndrome, since they may be predisposed to inordinate disability, symptom exaggeration, and high levels of health care utilization.
Malingering
Factitious disorder is driven by the aim to assume the role of being ill, impaired, or injured but without any obvious external rewards for such behavior (99). This aim has been understood to be driven by the internal reward received by obtaining sympathy, nurturance, or attention by assuming the sick role. It is distinguished from malingering, which involves the intentional reporting of symptoms for personal gain/reward (such as disability payments or avoidance of an unpleasant situation). The distinction is not always clear. While both result in the conscious/intentional feigning or physical production of symptoms; the motivation or decision-making process to produce these symptoms is fully conscious in the malingering person (who thus can be held accountable for their actions); while on the contrary, the motivation or decision making is instead unconscious and not intentional in the factitious patient—and thus is due to psychiatric disease. Malingering is not a somatoform disorder, not a form of psychogenic pain, and not a diagnosable disorder. It is simply a form of fraud that uses faux illness to obtain benefit. It is included in this section because it may be confused with or conflated with somatic symptom and related disorders such as factitious disorder, and because when symptoms seem inexplicable, malingering, somatization, and factitious processes are in the differential diagnosis. It is generally considered to be rare in patients reporting CNCP, but this belief may be based less on objective data than on the clinician’s need to believe patients in order to function well as a caregiver and advocate.
The burden of proof must be on the clinician to demonstrate the presence of conscious, willful motivation and deception prior to labeling a patient a malingerer, and for most conditions, that can only be accomplished through covert or overt observation. It is difficult to make this distinction, since it relies primarily on patient intent and consciousness of the situation, which are not readily observable. Surveillance may be the only way to diagnose some cases accurately, though grossly discordant findings (e.g., a person with prolonged inability to tolerate hand touch due to allodynia who has calluses and grease under the nails) suggest malingering.
Malingering is not rare in people seeking external gain, and many of us have been chagrinned to receive a surveillance video from a workers’ compensation case manager showing the crippled patient we have been caring for easily pushing a lawn mower.
Mailis-Gagnon et al. (102) reported that 4/15 women referred for presumed complex regional pain syndrome (RSD) had self-inflicted illness, characterized by limb ligation, ulcers, and “bizarre migrating wounds” that abated with casting. Other studies have shown a not-negligible prevalence of malingering in patients reporting pain (103), diarrhea (104), deafness (105), and cognitive dysfunction (106). Gervais et al. (107) found that fibromyalgia patients who were receiving or seeking disability income were likely to demonstrate faking on tests of memory complaints, in contrast to rheumatoid arthritis patients and fibromyalgia patients who were not seeking or receiving disability income.
Addiction
Because of the high prevalence of comorbid chronic pain and addiction and the fact that each condition complicates the diagnosis and treatment of the other, a separate chapter in this volume is devoted to the topic. It is included here only as a reminder that this illness is intimately involved with chronic pain, of which it can be a cause or consequence. It often goes unrecognized by the practitioner and the patient. At times, even the family may fail to appreciate the problem, as they mistakenly attribute addiction-induced impairments in mood and function to pain.
THE ROLE OF THE ENVIRONMENT
Environmental factors impact pain (and “pain behaviors”) in two primary ways: stressors influence the amount of pain experienced in a given situation, and incentives influence the pain experienced and the behaviors associated with it.
Stress
Stressful environments and experiences not only appear to magnify pain (hyperalgesia) but may generate it de novo. Rivat et al. (108) found that repeated social defeat induced hyperalgesia in rats that was associated with expression of proinflammatory genes (iNOS and COX-2) in the spinal cord. The effect was reversed by an antagonist of cholecystokinin, a transmitter in the descending pain facilitatory system. Le Roy et al. (109) demonstrated that nonnociceptive stress in rat models, especially if repeated, predisposed to development of hyperalgesia in response to pressure and inflammation. Green et al. (110) found that rats exposed to unpredictable sound stress developed an enhanced and prolonged response to cytokine-induced mechanical hyperalgesia, cutaneous and masseter hyperalgesia, as well as visceromotor hyperactivity and anxiety, thought to be reminiscent of fibromyalgia.
Human studies tend to focus on more extreme stress, such as that associated with combat. Chronic diffuse pain is one constellation of symptoms commonly reported in Gulf War veterans and is closely associated with psychiatric symptoms (111). Ginzburg and Solomon (112) compared 1982 Lebanon War veterans who had “combat stress reactions” (CSR) to a control group of veterans. Subjects were assessed at 1, 2, 3, and 20 years. CSR symptoms correlated highly with somatization and tended to predict it. Both groups of symptoms resolved incompletely over 20 years. As previously noted, extreme trauma is associated not only with unexplained somatic symptoms, including pain, but also with affect dysregulation and dissociation (102). Stress, of course, not only amplifies pain but also has the potential to create incentives for pain behaviors (v.i.) when such behavior provides escape from stress.
Behavioral Contingencies
“Operant conditioning” refers to the process in which reinforced behaviors increase in frequency and those not reinforced “extinguish.” It also includes effects of punishment. An essential perspective is the observation that survival requires this form of learning. An animal must repeat behaviors that lead to acquisition of food, water, and a mate in preference to those that failed to produce a “reward.” Key points regarding operant conditioning include the observations that (a) it often occurs without the knowledge of the trainer or trainee; (b) in most cases, repetition is required for conditioning to occur, so that the concepts are more important in chronic conditions than acute ones; and (c) the timing of reinforcement is critical. An immediate small reinforcer may outweigh a delayed large one, as reflected in the human penchant for behaviors that produce immediate small rewards despite substantial delayed adverse consequences. Addictive behavior may be driven at least in part by this phenomenon.
Because of conditioning, “illness behaviors” may become contingent on incentives and may increase or decrease regardless of nociception. It may be counterintuitive to posit that pain behaviors can result primarily from rewards, given that the life of the person disabled with chronic pain seems to provide remarkably few reinforcers. Poverty, depression, and loss of identity, friendships, and recreational activities are common. Nevertheless, much maladaptive behavior is maintained by initial consequences that are rewarding. For example, rest and inactivity provide initial relief, but over time, the resulting deconditioning increases pain.
The idea that “pain behaviors” (e.g., medically focused conversation, limping, rubbing body parts, and regression) can be maintained by external reinforcers led to efforts to reduce those maladaptive behaviors by not responding to them and, instead, reinforcing incompatible behaviors, such as speed walking. The first US program based on this model was designed by Wilbert Fordyce. Results were startling, as individuals who had been disabled began to exercise, relinquish assistive devices, and engage in conversations about non–pain-related topics (113,114). The operant conditioning–based program developed by Fordyce was soon emulated by hundreds of programs in several countries. The response of severely dysfunctional individuals to environmental contingencies in these programs has lent support to the belief that much unnecessary functional impairment is maintained by environmental rewards.
Disability as Pain Behavior
Pain-related disability, far from being an objectively determined medical condition, is strongly influenced by incentives and disincentives for vocational recovery. Positive reinforcers (caretaking, drugs, income) may be less important than “negative reinforcers,” such as the avoidance of a layoff or of noxious or hazardous work situations. While disability income is often meager, it is not contingent on one’s ability to compete in the work marketplace or on the viability of one’s industry in precarious economic times.
So-called secondary gain (external gains that accrue due to illness or symptoms) may increase pain behavior (115). In a comparison of 3,802 pain patients and 3,849 controls, Rohling et al. (116) found that financial compensation was associated with greater pain and reduced medical and surgical treatment efficacy. Even with such objective pathology as radicular pain due to acute disc prolapse/protrusion, the only predictive somatic factor was the degree of disc displacement—the less the displacement, the worse the outcome (117). Persistent pain was predicted by depression and coping strategies. Application for retirement at 6 months was best predicted by depression and daily hassles at work. On the other hand, when the incentives for wellness are powerful, function may be preserved despite serious illness. In a study of injured workers, return to work correlated strongly with preinjury wages, both in those who underwent spine surgery as well as those who did not (118).
The term “solicitous spouse” has been used to refer to the partner who, for example, waits on the patient unnecessarily, speaks for him/her, provides massages, and caresses the patient during the clinical interview. Pence et al. (119) reviewed studies of the impact of spousal behaviors (typically characterized as solicitous, punishing, or distracting) on patients’ activity level, pain, and mood. Additionally, they studied 64 headache patients by means of a self-report questionnaire. Patients reporting that their spouses responded negatively to well behaviors had more pain and pain behavior. Spousal responses judged to facilitate well behavior had no observable effect. Solicitous responses were associated with more pain, pain behavior, depression, and pain interference with life activities.
In a study of data recorded from home accelerometer monitoring of new patients in a chronic pain clinic, Alschuler et al. (120) examined pain sensitivity, fear avoidance, and solicitous spousal responses. They found that the operant conditioning model accounted for the preponderance of variance in physical activity. Patients were more active when spouses were less solicitous, less punishing, and more distracting.
Incentives for illness may also modify the family’s behavior, a phenomenon referred to as “tertiary gain.” For example, the wife of an unskilled worker in a floundering industry may sense that the family’s security is contingent on his disabled status. She therefore may defend his disability and support his helplessness. A particularly insidious form of tertiary gain is seen in the not uncommon situation in which a patient with chronic pain receives many hours of care per week from a “home health aide,” who happens to be a family member. The family member has income only so long as the patient remains unable to function.
Raichle et al. (121) briefly reviewed literature regarding the impact of spousal behaviors on patients with chronic pain and used the Spouse Response Inventory to study 94 patients scheduled for admission to a multidisciplinary pain program. They found encouragement of “well behaviors” to be related to lower levels of patient-reported pain behaviors, while negative responses to well behavior were associated with physical dysfunction. Both negative and solicitous responses to pain behaviors were related to poorer patient functioning. The literature is sufficiently consistent that we are now able to provide data-based recommendations to patients’ families as to how they can increase their loved one’s comfort and quality of life.
The impact of reinforcement on behavior begs the question of whether it also modifies perception. Flor (122) studied patients with chronic back pain and found that the presence of a solicitous spouse was associated not only with increased pain reports in response to electrical stimulation of the back but also with increased activation of pain- sensitive cortical areas, as reflected by EEG. Thus, it seems probable that reinforcing pain behavior can actually increase its perception. In support of this is the finding of Hölzl et al. (123) that reinforcement and “punishment” (through lower/higher thermode temperatures) carried out unbeknownst to subjects led them to either sensitize or habituate to a painful stimulus.
A focus on rewards that result from the sick role can foster the mistaken impression that people disabled by pain are somehow fortunate. In reality, most have sustained major losses, including friendships, the camaraderie of coworkers, pride in being the breadwinner, a sense of identity, and the self-esteem that comes from being a contributor rather than a burden to society and to one’s family. While disability income may provide security, it often does so at the poverty level. Thus, unsurprisingly, depression is rampant in this population.
Societal Issues
Some of the contingencies that modify pain behavior, disability, and presumably pain perception are beyond the control of families and health care providers. For example, workers’ compensation systems were designed to ensure medical care and supplemental income to those injured at work, and the system seems to work well when there is an objective loss, such as an amputation or loss of vision. However, in the case of a subjective “injury,” such as chronic pain, the system may inadvertently incentivize invalidism. A worker may need to “prove” how sick he is for months in order to receive the consultation or imaging he believes that he needs.
It has seemed to the members of our staff that as particular industries in our region were floundering, we would see an increased number of disabled workers from the industry affected. A worker who is disabled will likely have access to long-term subsistence wages and health care, while one who loses his job to downsizing quickly loses both. We did not sense that workers were feigning pain in order to abandon a sinking ship; however, the disincentives to rehabilitation that impacted middle-aged manual workers in a declining economy were considerable. For many disabled employees, access to health care may be contingent on remaining disabled, since the disabled person with pain who struggles to resume work may find no opportunities for full-time work with benefits. Disability income, in contrast, may be associated with health care for the patient and family.
There is a long and unresolved controversy concerning the role of litigation and compensation seeking in chronic pain, with many authors believing that these pursuits impede recovery. Indeed, these factors appear to be associated with worse outcomes; however, Spearing et al. have summarized the literature regarding these beliefs and note that studies showing a correlation between compensation seeking and poor recovery fail to control for reverse causality, that is, the likelihood that poor recovery leads to compensation seeking. Their statistical correction for this suggested that, when known additional factors are controlled for, seeking compensation may actually be associated with improved outcome (124,125). The authors additionally found that studies had been unable to control for the possibility of selection effects due to other factors. Intuitively, we might expect, for example, that those victims of a rear-end collision who are enraged might be both less likely to recover (see discussion re blame) as well as more litigious than those whose injuries do not provoke anger. Similarly, individuals with lower socioeconomic status or severe job dissatisfaction could be at risk for poor outcome and compensation seeking. Thus, at present, we are unable to conclusively determine whether seeking compensation per se alters the outcome of those with CNCP. We do, however, have compelling evidence of propensity of incentives and blame to increase pain and functional impairment.
DEVELOPMENTAL ISSUES
It has long been thought that adverse childhood events promote somatization, psychogenic pain, and psychogenic exacerbation of pain from illness or injury. Major factors implicated have included (a) abandonment, neglect, and insufficient nurture and (b) physical or sexual abuse (126–131).
Using a structured biographical interview, Imbicerowicz et al. (132) compared the childhood experiences of controls (medically explained chronic pain) with patients with fibromyalgia and with somatoform pain. They found that the latter two groups had more childhood adversities, including sexual and physical maltreatment, poor emotional relationships with parents, lack of physical affection, parental quarreling, substance abuse in the mother, separation, and financial stress, prior to the age of 7. Mallouh et al. (133) studied the effect of loss on treatment outcome in 92 “persistently somatizing” inpatients. Those with early loss (loss of a parent before age 17) were compared with those recently (2 years) bereaved and those with no loss. Early loss was associated with worst outcome, poor social adjustment prior to treatment, and a greater incidence of dependent personality disorder. Bereaved patients responded best to treatment.
Brown et al. (134) compared 22 patients with a diagnosis of somatization disorder and 19 medical comparison subjects using structured interview instruments. Somatization disorder patients reported significantly more childhood emotional abuse, family conflict, and more severe forms of physical abuse and less family cohesion. Chronic emotional abuse was the best predictor of unexplained physical symptoms. Sexual abuse, separation/loss, and witnessing violence were equally common in the two groups. The somatization disorder group reported significantly more family conflict and less family cohesion.
Sachs-Ericsson et al. (135) studied 5,877 subjects who received Part II of the National Comorbidity Survey in the 1990s. Those with current (12 months) health problems were asked about their current pain. Those with abuse histories reported more pain, and the difference was not explained by depression. Landa et al. (136) have reviewed evidence that childhood neglect and trauma are associated with later life somatization. They cite a convergence of information from genetics, developmental neurobiology, and other fields, suggesting that there may be a shared neural system underlying physical and social pain and that this system can be disrupted by deficiencies in the early infant/ caregiver relationship.
Support for these conclusions has been found with experimental pain in humans and animal models. In women with and without irritable bowel syndrome, Ringel et al. found that a history of abuse predicted increased pain and anxiety in response to rectal distension. Additionally, there was greater activation in the left posterior and middle dorsal cingulate subregions. Those with both irritable bowel syndrome and abuse showed the greatest degree of pain and cingulate activation. Activity in the left supragenual anterior cingulate, an area that has been associated with inhibition of pain and arousal, was diminished (137).
Coutinho et al. (138) exposed rat pups for 3 hours/d to maternal separation on postnatal days 2 to 14. At 2 months of age, they showed increased visceromotor responses to colorectal distension and increased stress-induced fecal pellet output, suggesting that the early stress/deprivation predisposed to visceral hyperalgesia and increased colonic motility in response to psychological stress. In another investigation, neonatal rats were stressed on days 2 to 9 of life by having limited bedding in their cages. As adults, they demonstrated lower mechanical nociceptor thresholds in skeletal muscle and prolonged hyperalgesia following prostaglandin E2 administration (139).
The mechanisms through which deprivation, neglect, and abandonment in childhood could lead to physical symptoms are unclear; however, one line of investigation points to insecure attachment as a prominent factor (140), and increased vigilance and anxiety may also play a role (141).
Since psychological trauma, including neglect, induces neurologic changes that promote pain, we must question whether the term “psychogenic” still applies. Rome and Rome (142) speculated that psychologic trauma, in a process akin to kindling, can evoke a hypersensitivity not unlike that seen in neurogenic sensitization and that this hypersensitivity involves cross-sensitization, so that the individuals are hypersensitive to psychic (loss, humiliation) and physical (injury) trauma, both of which elicit both physical and affective symptoms. They coined the term “polymodal allodynia,” which seems to describe well the vulnerability experienced by these patients.
IDENTIFYING PSYCHOLOGICAL CONTRIBUTIONS TO PAIN
It is likely that all pain and pain behavior are modulated to some extent by psychological factors. Mood, expectations, fears, cognitions, and contingencies impact all people and thus their pain and pain-related dysfunction. People describe symptoms differently to their mothers than to their drill instructors. Functional impairment is portrayed differently by people trying to obtain employment than by people trying to demonstrate disability. So while these factors modulate pain, they do not rule out an organic source of pain, even when the psychological issues are marked. Perhaps the most straightforward psychological influences to identify are those related to mood, anxiety, and substance use, given the relatively objective criteria for their presence.
Emotional symptoms, including depression, anxiety, and irritability, should be noted, along with such symptoms as crying spells and changes in sleep, energy, interest, libido, humor, concentration, appetite, and weight. Suicidality should be assessed. Anxiety and panic attacks should be noted. PTSD is suggested by reexperiencing symptoms, such as flashbacks, nightmares, and intrusive recollections; anxiety or hypervigilance with increased startle response; and efforts to avoid situations reminiscent of the original trauma.
It is advisable that every patient seen for chronic pain undergo at least a brief screening for the presence of anxiety and depression. There are numerous instruments for this purpose, validated in a variety of populations, some of which are available without cost. The Patient Health Questionnaires can be used and printed without permission and have been demonstrated to have good psychometric properties (e.g., 143,144). The PHQ-9 for depression and the GAD-7 for anxiety are quite useful, and they have been supplemented by 2-item questionnaires (PHQ-2, GAD-2) that may be combined into the PHQ-4 to screen for both anxiety and depression in a busy practice. Instruments, scoring instructions, and a bibliography are available at www.phqscreeners.com.
The presence of substance use disorders is somewhat more difficult to diagnose in those with chronic pain, at least when the substances involved are obtained legitimately for symptom control. The chapter in this text that addresses pain and addiction has more information on making this diagnosis, but again, it is reasonable to question all patients with chronic pain as to whether medical or other substances have ever become a liability for them and perhaps to ascertain whether cohabitants agree.
The diagnosis of a somatic symptom disorder may be more challenging, since some judgment is involved in the determination as to whether there are “excessive and disproportionate thoughts, feelings, and behaviors” regarding the symptoms. Multiple somatic complaints may be one clue. Although it is clear that a multiplicity of pains predicts more pain (38), this could result from genetically determined reductions in pain perception. Dworkin et al. (145) found that a multiplicity of pains correlated with levels of somatization as reflected on the SCL-90R (Symptom Checklist 90, Revised). Streltzer et al. described detailed psychiatric evaluations of 54 injured patients who were either litigants or seeking workers’ compensation benefits. In comparison with those who did not develop a somatoform pain disorder, those who did had more areas of pain, pain spread beyond the area of injury, more use of benzodiazepines and opioids, and appeared to be more influenced by compensation and litigation factors (146). (As a caveat, it should be recalled that symptom spread beyond the area of injury occurs in animal models, perhaps mediated by glial activation, and that “nonphysiologic findings” conceivably could reflect the fact that neurophysiology is not fully understood.)
Disproportionate responses to pain may be present when patients rate their pain greater than 10 on a 0 to 10 scale or choose more than 21 pain descriptors on the McGill pain questionnaire (where 21 is the maximum score). Those whose pain drawing (a human figure on which the patient is asked to shade regions of pain) contains multiple, unrelated pains and pains extending outside the body may be demonstrating inordinate pain behavior.
Inconsistencies may provide an important clue to the presence of impairments that are not fully neurologically based. Symptoms should be consistent with some known disease or group of diseases. Strength should be consistent, whether assessed by gait, toe/heel walking, or manual muscle testing. Limping, use of assistive devices, and pain behavior should be not contingent on the audience. Functional impairment should be consistent with pathology; for example, a person with LBP whose questionnaires are completed by a spouse or who looks to a spouse to explain the characteristics of his/her symptoms may be demonstrating inordinate regressive behavior. An orthopedic lesion causing knee pain is unlikely to fully explain vocational disability in a sedentary worker. The weakness of these statements, however, resides in the fact that severe pain can interfere with concentration sufficiently to impair the function of a person in ways unrelated to the function of the injured body part.
The evaluation of a seriously impaired person with CNCP should always include an assessment of function. A rating scale, such as the Pain Disability Index (147), may be the easiest way to accomplish this while also establishing a useful baseline against which to assess treatment effectiveness. A brief assessment of the patient’s environment should include inquiry regarding significant stresses, incentives for recovery, and those for being disabled.
PSYCHOLOGICAL APPROACHES TO THE TREATMENT OF PAIN
Physical Reconditioning
Exercises and physical therapy have been shown to improve pain and function in those with CNCP (148,149), but physical therapy can also be conceptualized as a critical form of psychotherapy in this population. Deconditioning fosters a sense of helplessness and fragility. It causes activities to become more painful, thus limiting access to sources of fulfillment and pleasure and promoting depression. Fear is a major contributor to deconditioning, and physical therapy becomes a form of systematic desensitization that reduces patients’ sense of fragility (150). It is a powerful antidote to “learned helplessness” and directly reduces symptoms such as anxiety and depression (151–153). Fitness promotes activities that distract from pain while improving self-esteem. It may be useful to have family members witness exercises, since they may become less “enabling” when they no longer see their loved one as fragile and helpless. Numerous studies support the role of exercise in chronic back and neck pain, but the studies tend to be weak (154–157). Remarkably, Brox et al. (158) were able to randomize patients with so-called failed back syndrome to treatment either with exercises plus education or with lumbar fusion. Outcomes were virtually equal.
Physical therapy modalities are less clearly beneficial. Although some evidence supports the effectiveness of therapeutic massage (159,160), many studies fail to show benefit (161). Modalities should be used with caution because of their implicit message that improvement results from being a passive recipient of others’ ministrations, rather than through personal efforts.
Education
People’s understanding of the significance of their pain influences the attention paid to it, their level of vigilance, and the extent to which pain limits activities. If pain signifies that “The exercises must be tearing something loose,” the response will be very different from that if it signifies, “I’m not working out often enough.” Roth et al. (162) found that those who believed their chronic pelvic pain had a serious import had greater pain severity, more suffering, and more functional impairment. In muscular dystrophy and facioscapulohumeral dystrophy, Nieto et al. (163) showed that changes in pain beliefs predicted changes in pain intensity as well as in physical and psychological function. Pons et al. (164) studied 144 participants in exercise and education programs provided by the Arthritis New Zealand. This cross-sectional study found that “organic pain beliefs,” for example, that pain is an indicator of bodily harm, that the amount of pain reflects the amount of damage, and that exercise makes pain worse, were associated with poor function.
When patients are bewildered about the cause of their pain, suffering and dysfunction are magnified. It is therefore essential to reduce mystery and uncertainty when possible (165). Waddell et al. (166) found that disability due to back pain was better accounted for by fear avoidance beliefs than by pain itself. In their study, the most harmful beliefs related not to disease severity but to uncertainty regarding diagnosis. Such an association is a special challenge in caring for patients with chronic LBP, for which a precise anatomic explanation is typically unavailable.
Teaching should include the pain pathology, if known, the fact (when true) that it is not an indicator of fragility, a threat to body integrity, or a sign of progressive degeneration, and the difference between hurt and harm, so that patients are not deterred from reconditioning programs that may initially hurt.
Education also should include families, lest they promote unwarranted regression. “Enabling” behavior commonly results from misunderstanding the nature of the pain, which activities are harmful, and which are helpful. It may be useful to discuss such concepts as central sensitization, hyperalgesia, and genetic influences on pain perception as a basis for a discussion about the fact that pain can be both real and severe in the absence of peripheral pathology. It is important to keep in mind that “They can’t find the cause of my pain” is an idea that is associated with increased pain, self-protection, and functional impairment and is an impetus to perpetuate futile medical investigations.
Much maladaptive behavior on the part of patients and families can be understood as an inappropriate extension of appropriate acute pain management into the chronic phase, so that the regression and caretaking that initially protected injured parts and promoted healing come to promote deconditioning, increased pain, and impaired quality of life. Families should understand that the worst treatment is rest and that activity is beneficial.
Cognitive–Behavioral Therapy
The term cognitive–behavioral therapy (CBT) subsumes a number of different cognitive therapies, relaxation training, and behavior therapies.
Cognitive Therapy
In classical CBT, patients are trained to identify, challenge, and alter thinking patterns that tend to be automatic and distressing, while at the same time reducing self- defeating behaviors (167). The goals of CBT typically involve improved pain tolerance, decreased emotional distress, and functional restoration. Most approaches share the principle that emotional reactions are determined by thoughts and perceptions rather than by events per se, and this principle is thought to apply to pain as well. Therapies are typically time limited and somewhat didactic in structure with homework assignments.
As an example, a patient may be worried about his LBP and unsure what it portends. (Patients’ interpretations of such explanations as “Your spine is degenerating” can lead to considerable fear.) If he sits up and has a sudden pain, it may (a) be amplified by hypervigilance and (b) lead to such conclusions as “I must be getting up too soon. Perhaps I should rest a few more days or spend the day in the recliner.” This decision, based on erroneous conclusions, promotes deconditioning, anxiety, avoidance of pleasurable and productive activities, depressed mood, and a focus on somatic themes that can alienate those who might otherwise seek his company. The loss of social contacts, in turn, leads to feelings of abandonment and betrayal. An alternative thought process could be “That really hurt, but most of the pain is probably muscular; after all, everyone’s spine is degenerating after the age of 23, and there are 70-year-olds who run marathons. Perhaps some stretches will help. In any case, the pain always diminishes eventually. In the meantime, going for coffee with a friend might provide a distraction.” It is obvious how inaccurate cognitions can lead to a cascade of emotional and behavioral changes that disable and demoralize the sufferer.
In CBT, “learned helplessness” and “external locus of control” can be replaced with the mind-set that the patient is in charge of his life. Thoughts that “the exercises are damaging my back” can be replaced with “the pain I’m having now probably means that I need to exercise more.”
Studies show that CBT leads to improvements in activity, psychological function, pain, and medication use (168). A meta-analysis of 25 controlled trials confirmed the efficacy of this therapy for pain, mood other than depression, social function, and pain behavior (169).
Glombiewski et al. (170) performed a meta-analysis of psychological treatments for fibromyalgia and found robust but small effect sizes. Medium effect sizes were found for CBT. In the case of neuropathic pain, Wetering et al. (171) found limited evidence of efficacy for pain reduction, although other components of the pain syndrome were improved. They noted that many studies were small pilot studies. Hoffman et al. (172) in a meta-analysis of 22 studies of psychological interventions for LBP found strong support for the benefit of CBT in reducing pain; however, self-regulation therapies (e.g., relaxation training and biofeedback training [BFT]) were superior for reducing depression.
Mindfulness
Techniques for meditation have been used for millennia; however, their scientific investigation largely derives from early work of Herbert Benson, who documented dramatic reductions in physiologic stress responses in practitioners of various forms of meditation. His book, The Relaxation Response (173), became popular among lay readers and presented meditation as an antidote to the “fight-or-flight” response. He coined the term “relaxation response,” which is the converse of the stress reaction and which can be elicited by such techniques as deep breathing exercises, guided imagery, meditation, progressive muscle relaxation, yoga, and tai chi. Listening to a CD designed to elicit the relaxation response was recently shown not only to reduce perceived psychological distress in novices and long-term practitioners but also to produce reductions in cortisol, ACTH, and norepinephrine during the listening period in the experienced group (174).
CBT has evolved over the years and increasingly focuses on such concepts as mindfulness and “acceptance and commitment therapy” (ACT). In part, these concepts and their associated therapies embody a recognition that the quest for a cure of illness and elimination of symptoms can become self-defeating and ultimately constitute a part of the problem. The newer work holds that there can be value in surrender and that symptom control strategies can be harmful if they fail, dominate the person’s life, or lead to loss of valued activities and goals (175). In 105 chronic pain patients, McCracken et al. (176) found that baseline mindfulness, as reflected in the Mindfulness Attention Awareness Scale, was associated with reduced depression, pain-related anxiety, and both physical and psychological functional impairment. There is early evidence that mindfulness and acceptance correlated with improved function and reduced opioid use in patients with chronic LBP (177).
Zeidan et al. (178) extensively reviewed the literature related to pain and mindfulness, which they characterized as including (a) regulated, sustained attention to the moment-to-moment quality and character of sensory, emotional, and cognitive events, (b) the recognition of such events as momentary, fleeting, and changeable (past and future representations of those events being considered cognitive abstractions), and (c) a consequent lack of emotional or cognitive appraisal and reactions to these events. Mindfulness is taught by one of several forms of meditation training. Although it originated in the Buddhist tradition, contemporary training is usually fully secular. Zeidan’s group found compelling support for the ability of both “focused attention” and “open monitoring” forms of meditation to reduce both the perception of pain and its associated unpleasantness. Further, they reviewed imaging studies demonstrating differences in regional brain activation in meditators versus nonmeditators on exposure to noxious stimuli. The amount of training required to produce meaningful differences in pain perception was as small as 4- to 20-minute sessions.
Interestingly, Cassidy et al. found that mindfulness increased in patients with chronic LBP following a 3-month cognitive–behavioral multidisciplinary pain management program. Mindfulness predicted lower levels of disability, anxiety, depression, and catastrophizing, and it appeared that the relationship between mindfulness and disability was mediated by catastrophizing. Similarly, Baranoff et al. (179) found that changes in acceptance, which was not specifically targeted, predicted changes in depression and physical function in 128 patients treated in a 3-week multidisciplinary pain program. Thus, it appears that cognitive–behavioral interventions affect both catastrophizing and mindfulness. These studies support the idea that catastrophizing is the converse of mindfulness (180).
Acceptance and Commitment Therapy
ACT combines acceptance therapies with a focus on behaving in ways that promote valued goals, rather than behaving in the service of avoidance of discomfort (181,182). In a small study of 11- to 18-year-olds, Wicksell et al. compared the effectiveness of an ACT-oriented intervention with multidisciplinary treatment including amitriptyline. Ten weekly sessions of ACT were superior in improving pain, fear of reinjury, interference, and quality of life (183).
In a meta-analysis of 22 acceptance-based studies, including mindfulness and ACT, Veehof et al. found evidence of efficacy for pain (effect size 0.37) and depression (effect size 0.32). Benefit was also found for anxiety, physical well-being, and quality of life. The authors concluded that, although results were not as strong as those supporting CBT, the acceptance-based treatments were a viable alternative to them (184).
Though these new areas of study have not been fully vetted, they are promising and congruent with clinical observations that patients who accept the idea that, since chronic pain is rarely eliminated for long, they will choose to have a good quality of life despite it, are the ones who feel and function best over time.
Assertiveness Training
Few studies are available to test the hypothesis that assertiveness training is a valuable adjunct in the treatment of disabled patients with chronic pain, yet there is a long tradition of incorporating this modality into CBT, perhaps especially as provided in interdisciplinary chronic pain programs (IPRPs) (185). Poor skills in communicating one’s needs, difficulties resisting the demands of others, and tendencies to feel victimized in interpersonal encounters can create strong incentives for the “sick role.” Needs for closeness and caretaking can be expressed through somatic complaints. Pain can become an excuse for saying no when people lack the skills and confidence for refusing gracefully. And cultural proscriptions of unkindness to the sick may buffer the nonassertive against others’ insensitivity. Assertive training provides alternative strategies that facilitate relinquishing the sick role.
Patients, especially passive ones, may have concerns that assertive training will encourage them to be demanding or unpleasant. It is and should be presented as a strategy for being honest about one’s needs and reactions in a way that is respectful of others. For example, the assertive alternative to “You’re a jerk,” or “Whatever you say” might be “I feel angry when you talk to me in that tone of voice, and I’d prefer that you communicate your point in a kinder way.” A slogan in this area is, “Say what you mean, and mean what you say, but don’t be mean when you say it.” As patients set limits on how others treat them, what they’re willing to do, and communicate their needs, the sick role becomes less necessary.
Biofeedback/Relaxation Training
Clinical BFT seeks symptom control by using electronic feedback to teach patients to regulate body functions that are not usually under voluntary control, such as skeletal muscle tension, palmar sweating, gastrointestinal motility, and digital blood flow (186). It has proved useful in areas unrelated to pain, such as sphincter control following neurologic injury and anxiety disorders, among others. Training in warming the extremities is helpful in Raynaud syndrome (187) and may reduce hypertension (188). It is commonly used to train autonomic responses in complex RSD (reflex sympathetic dystrophy) (189). Electromyography (EMG) training to produce frontalis relaxation has been used in tension headache, fibromyalgia (190), and back pain (191). Masseter feedback may be useful for temporomandibular joint syndrome (192). EMG BFT was shown to speed rehabilitation following meniscectomy (193). The indications for BFT are not fully defined and continue to expand into conditions as diverse as rectal pain (194), cumulative trauma disorder (195), and vulvodynia (196,197).
Scientific confirmation of the benefits of BFT has proved difficult. In part, this may be because BFT is typically provided in combination with various other techniques, such as progressive muscular relaxation, meditation, guided imagery, or self-hypnosis training. In part, it is difficult to study because comparators in studies are themselves effective (e.g., guided imagery).
A Cochrane study of psychosocial interventions for chronic orofacial pain found difficulty in determining treatment efficacy due to heterogeneity of interventions and outcomes, likelihood of bias, and treatments commonly provided in various combinations (198). The authors concluded that there was only weak evidence supporting behavioral psychosocial interventions to improve long-term outcomes in chronic orofacial pain, although effects were significant for improvement in long-term pain and depression. Evidence was best for CBT, which, either alone or in combination with biofeedback, resulted in long-term improvement in activity interference, pain, and depression.
Both EMG and thermal biofeedback have been used extensively in tension and migraine headache (199–203); however, a recent study of 64 migraineurs found that it did not add to the benefit produced by relaxation training alone (204). Improvement occurred in 52% and 57%, respectively. BFT may potentiate the effect of pharmacologic treatment, as suggested by a randomized controlled trial (RCT) in which it was combined with β-blocker prophylaxis (205).
In an RCT of 60 female Swedish service organization workers disabled with neck pain, Dellve et al. (206) found that trapezius EMG feedback produced pain relief, while strength training increased ability to work. Ma et al. (207) found that BFT was superior to both exercise and passive PT modalities in computer workers with neck and shoulder pain. Yet an RCT of 65 patients with chronic whiplash pain found no efficacy of EMG BFT (208).
BFT has been evaluated in several studies of chronic LBP with contradictory findings. In disabled workers, Neblett et al. (209) found that EMG-assisted stretching led to normalization of the abnormal paraspinal muscle tension typically seen during lumbar flexion in those patients. Recently, in an RCT of 128 highly disabled patients, Glombiewski et al. (210) found that CBT was helpful, as was CBT + BFT; however, the addition of BFT provided no demonstrable benefit. It should be noted that the CBT alone group received training in progressive muscular relaxation.
BFT has been studied extensively in pelvic pain syndromes. In 140 cases of chronic prostatitis/chronic pelvic pain syndrome, Yang et al. (211) found that BFT, with and without combined electrical stimulation, produced improvements in pain, urinary symptoms, and quality of life. Recently, in 157 patients with levator ani syndrome, Chiarioni et al. found it superior to massage and electrogalvanic stimulation, with 87% responding and a mean pain reduction of 74%. Results were largely maintained at 1-year follow-up.
Recent studies indicating that pain is associated with a relative increase of EEG beta-wave activity and a decrease in slower frequencies has led to speculation that EEG biofeedback (“neurofeedback”) may have a general pain-lowering effect. An early (open) study in fibromyalgia supports this (212). Stokes and Lappin (213) evaluated the additional benefit of 40 neurofeedback sessions (three different types of biofeedback: EEG, hemoencephalography, and thermal hand warming) in 37 migraineurs receiving various preventive drug treatments and found that neurofeedback reduced migraine frequency by 20% compared to medication alone.
Clinical experience is that patients rate BFT one of the most helpful interventions in a multifaceted, interdisciplinary program. Perhaps this is because, in addition to it specific benefits, biofeedback helps skeptical patients understand the relationship between external and internal events. A patient who witnesses a drop in hand temperature when discussing an employer may be convinced of the importance of stress management in modifying his or her body’s responses. Thus, BFT may facilitate work in other program components. Given the relatively weak and contradictory results of studies of BFT in chronic pain, it seems reasonable to conclude that it is helpful in a variety of pain syndromes that are incompletely defined; however, the benefit that it provides can usually be obtained without the need for physiologic monitoring equipment by using other techniques.
Behavior Modification
The management of CNCP has as much to do with changing behavior as reducing pain perception. Pain behaviors may be separated into those that primarily benefit nociception and function (using a heating pad, ankle orthosis) and those that primarily affect others (“pain talk”). Some behaviors, such as wearing a TENS device or corset outside clothing, may do both. Maladaptive pain behaviors tend to occur preferentially in the presence of others and include moaning, complaining, and holding body parts.
Behavioral change is produced when its environmental consequences change; for example, animals press a lever frequently when the result is food delivery, and they stop after a time if the delivery ceases. This process has been studied in intensive pain rehabilitation programs (IPRPs), where social reinforcers can be made contingent on healthy behaviors, while pain behaviors are ignored (214). Sanders (215) reviewed 30 studies, of which 15 were RCTs, and found strong support for operant conditioning as a treatment of chronic LBP. It led to significant improvement in function and activity along with reductions in both analgesic use and pain intensity.
Thieme et al. (216) randomized fibromyalgia patients to treatment with CBT, operant behavioral therapy, and a discussion group about fibromyalgia. Operant treatment (which included families) and CBT led to improvements in pain, emotional distress, and function at 1-year followup. Both led to improvements in cognitive variables (e.g., catastrophizing, maladaptive beliefs). CBT had a somewhat greater effect on affective distress and catastrophizing, while operant treatment had more effect on functional limitations, pain behavior, and solicitous spouse behavior. Operant treatment was the only one that led to a reduction in physician visits. Patients in the discussion group deteriorated.
In clinical practice, behavior modification typically provides the context in which multiple other treatments are carried out. For example, in physical therapy, praise, rest, and other “rewards” follow goal completion, rather than “trying.” During various therapies, somatic conversation can lead to loss of eye contact and interaction, while discussion of other subjects leads to eye contact, nods, and increased responsiveness.
It is apparent how contingency management alters behavior, but is less obvious how it changes pain perception and suffering. While some pain reduction may occur secondarily from behavioral activation, exercises, and distraction, Flor’s work suggests that avoidance of reinforcement for pain may directly decrease its perception.
Family Therapy
Those who share a home with people in chronic pain not only are impacted by the pain themselves but are also a major influence on the patient’s functional impairment and mood (217). The influences are bidirectional—living with a person who has chronic pain can stress the family emotionally and financially and often leads to family-wide reductions in recreation and socialization. The family is likely to feel obligated to take on the role of caretaker. Role reversal is common, and patients frequently express remorse for the fact that their small children have begun to parent them.
McCracken (218) studied 228 consecutive patients referred to an IPRP and confirmed that both solicitous and punishing responses from significant others were negatively associated with acceptance of pain. Raichle et al. (121) confirmed the marked effect of partner responses on function and mood. Encouragement of well behaviors was associated with fewer pain behaviors. Negative responses to well behavior were related to greater patient physical dysfunction. Both solicitous and punishing responses to pain behaviors were related to worse patient functioning. Negative responses to pain behavior were associated with more depression in the patients.
Alschuler et al. (120) equipped LBP patients with inertial activity monitors and investigated the relative influence of pain, fear/avoidant issues, and operant factors (family behaviors that were solicitous, punishing, or distracting) in predicting function. Family operant factors were the best predictors of physical activity. The authors suggested that training family members in operant principles could be a critical step in pain rehabilitation.
Based on these studies, we can reasonably conclude how families of patients should be counseled to behave. These people often report that they responded helpfully to their loved one’s acute pain until the transition to chronic pain occurred, and they no longer knew how to be helpful. They often perceived that the nurturing that facilitated acute healing was not leading to improvement and may have promoted invalidism, yet when they discontinued it, they felt guilty for being uncaring. Many report a sense that whatever they do is wrong.
Messages for Families
1. Support, validation, and positive regard are important.
2. Rewarding “pain behavior” promotes its increase; thus, positive statements and attention should be contingent on behaviors that are not intrinsic to pain or the sick role (e.g., comments about emotions or current life events should receive more response than comments about pain, medications, and treatments).
3. Overprotection promotes invalidism. Movements in the direction of normal behavior should elicit enthusiastic encouragement, not dissuasion and cautions. Offers to accompany the patient on an outing are a better gesture of affection than suggestions for rest in the recliner.
4. Criticizing “pain behavior” is likely to promote its increase while helping to engender depression.
5. It may be helpful to think in terms of reversing the role change to that of caregiver and replacing it with that of companion, friend, lover, or playmate.
A critical issue is that advice to ignore pain behaviors not be misinterpreted as advice to ignore the person. Many families of patients with chronic pain have found useful guidance in a manual for families that teaches these principles, published by the American Chronic Pain Association (ACPA) (www.theacpa.org).
The distress of family members often warrants specific management. They may find their lives controlled by a loved one’s illness. They feel duty bound to give, yet receive little. Self-blame and guilt coexist with resentment. They may feel helpless and depressed, and their own lives often become unmanageable. Family discord often becomes a major source of stress for the patient with pain. Individual counseling, group therapy involving family members of pain patients, and conventional family therapy have all been used with success. Restoration of good quality of life to the non–pain sufferers is a valid treatment goal.
Interdisciplinary Pain Rehabilitation Programs
Early IPRPs were modeled on the original behavioral program designed by Fordyce (v.s.); however, various combinations of interventions have been employed in subsequent treatment centers. Typical services in IPRPs include education, reconditioning physical therapy, medications, BFT, operant conditioning, psychotherapy (personal and family), medication weaning, addiction treatment, and treatment of psychiatric comorbidity. Interventions such as TENS, spinal cord stimulation, and nerve blocks may be included. Combined treatments appear to be more effective than unitary treatments for CNCP. Unless they exclude patients with substance use disorders, IPRPs should provide access to addiction education and treatment during the program. Such programs can dramatically improve the quality of life and functional abilities of disabled pain patients. In an early meta-analysis of 65 studies of IPRPs, Flor et al. (219) found improvements in pain, mood, and interference with life activities, including work. Health care utilization declined, and benefits were stable over time.
In 1996, Turk reviewed outcome studies of interdisciplinary programs and found pain reductions of 14% to 60%, opioid reductions of up to 73%, and dramatic increases in levels of activity (220). Forty-three percent more patients were working after treatment than before. One of his reviewed studies (221) found a 90% reduction in physician visits following treatment. There were 50% to 65% fewer surgeries in treated than in untreated patients and 65% fewer hospitalizations. Thirty-five percent fewer patients were on disability income supplementation. Turk estimated that IPRPs led to 27 fewer surgeries per 100 patients, for an average (in 1995 dollars) of $4,050 saved per patient (at $15,000 per surgery). He estimated overall medical costs at more than $13,000 per year pretreatment and $5,600 in the year after treatment. This suggests a savings of $7,700 per year per patient following treatment. Disability savings approximated $400,000 per person removed from permanent disability. More recently, Gatchel and Okifuji have reviewed studies of IPRP effectiveness and concluded that such treatment is the most efficacious and cost-effective, evidence-based treatment extant for CNCP (222).
In 2007, Turk and Swanson reviewed studies of the effectiveness and costs of a number of treatments for chronic pain and cited studies showing the mean pain reduction from IPRPs to be 37%, which occurred along with 63% reduction in analgesic use (223). In contrast to many treatments (e.g., stimulators, pumps, pharmaceuticals) that require substantial continuing health care utilization, IPRP treatment was typically associated with a reduction in health care and associated expenditures. IPRPs were two to four times more cost-effective than spinal cord stimulator or intrathecal analgesia for increasing physical function. IPRPs were shown to be 12 times more cost-effective than conventional medical care, 17.5 times more cost-effective than spinal cord stimulator, and 30 times more cost-effective than surgery for the goal of return to work.
Most studies of IPRP treatment have involved a broad mix of patients and conditions, but a few have addressed specific populations. For example, Darchuk et al. (224) studied treatment outcomes in patients ≥60 years old and found IPRP treatment to be as effective in this group as with middle-aged patients. In patients with whiplash, Angst et al. (225) found large effect sizes that were maintained at 6 months follow-up in pain, function, and quality of life. Patterson et al. (226) found IPRP treatment to be successful in reducing pain, depression, anxiety, and functional impairment in 45 patients with complex RSD. Busch et al. (227) recently found that even 10 years following completion of IPRP treatment, workers had reduced levels of disability than comparison groups who had physical therapy or CBT.
Not surprisingly, patients are often apprehensive that increased activity and reduced medications will increase their suffering, and often only the example of patients farther along in the recovery process encourages them to stay in treatment. Excessive sick role behavior can be conceptualized as similar to addictive behavior, in that patients compulsively behave in ways that produce immediate relief, but long-term increased suffering. They expect to suffer more when they relinquish their customary adaptive strategies, yet in fact they suffer less.
Self-Help/Mutual Support
A significant amount of psychological help and support can be provided to people with CNCP by self-help groups. They often provide accurate medical information, validation, and guidance in the direction of normalizing quality of life. The ACPA is a self-help recovery program for those with chronic nonmalignant pain (228). Its focus is on self- management. Members are encouraged to employ daily relaxation, stretching exercises, and such psychological tasks as working on goal setting, assertiveness, and avoiding pain behavior. The concept of changing “from a patient to a person” is emphasized. There are fewer than 400 chapters, so it may not be accessible to many. Materials are available to help persons with pain start new groups. ACPA does not focus on substance use, so treatment and participation in Alcoholics Anonymous or Narcotics Anonymous are also important for pain patients with co-occurring addictive disorders.
Chronic Cancer Pain
Although not the focus of this chapter, cancer pain warrants mention for several reasons: First, cancer has become a chronic disease, and thus most of the material in this chapter is relevant to those in prolonged remission. Additionally, most of the comments of this chapter regarding the importance of treating comorbid depression and anxiety and providing coping skills training can be applied to the cancer patient who is not acutely ill. Physical therapy directed toward maximization of strength and flexibility can reduce discomfort and improve quality of life, while providing distraction. Malignant pain, of course, often is cured and may transition into such chronic nonmalignant pains as toxic neuropathy or radiation cystitis, which are forms of CNCP.
CONCLUSIONS
Compelling evidence demonstrates that the boundary separating the psychogenic from the organic has become increasingly permeable and that psychological traumas can produce lasting alterations in central nervous system function and even structure. At the same time, studies have shown that numerous painful symptoms thought to be psychogenic have their explanation in central sensitization and neuroplasticity. Further, there is a constant interaction between the neurologic and the psychological, so that matters of salience and vigilance modify nociceptive transmission. Function, on the other hand, seems to be largely psychologically determined in these patients, given that there is essentially no correlation between tissue injury and function in long-term studies and that psychosocial issues have proven to be good predictors of function.
Many psychological interventions have been shown to be effective for reducing pain and improving function and mood. They are rarely curative, and we are left with the necessity to understand patients from both biologic and psychosocial frames of reference and to intervene with tools from both areas of study. Fortunately, the biologic and psychological tools are often synergistic, and patients, even with intractable pain, can be restored to full function and quality of life.
CASE STUDY 94-1
This 55-year-old manager had intermittent low back pain for 20 years that had become disabling for the last 2 years. Pain radiated to the left knee but was nonradicular. Imaging showed degenerative disc disease, facet arthropathy, and grade I spondylolisthesis at L4–L5.
He’d failed to benefit from moderate doses of hydrocodone and oxycodone with acetaminophen. Two epidural steroid injections had produced transient relief and were deemed not worth repeating.
He reported mild anxiety and moderate depression with reduced sleep, energy, and interest. There was no suicidal ideation or anhedonia, and humor was preserved. He’d gained 30 pounds in 2 years.
He denied nonmedical stresses beyond “the usual hassles” of a demanding job.
He had been missing several days’ work each month for over a year and, for 3 months, had been on sick leave. The Pain Disability Index score of 35/70 confirmed pain-related impairments in socialization, recreation, and sexual function.
His wife responded with considerable support and was protective of him. At times, he looked to her to answer questions regarding his symptoms and emotions, which she did.
Medical history and psychiatric history were significant for moderate obesity, hypercholesterolemia, hypertension, and prediabetes. There was no substance use history, including nicotine, beyond minimal social alcohol use.
There were no neurologic deficits. He had restricted lumbar range of motion and paraspinal muscle tenderness and tightness.
He was diagnosed with mechanical low back pain, degenerative disc disease, and spinal osteoarthritis. Based on the finding that his functional impairment, including regression in the marriage, was discordant with medical pathology, he was also thought to have pain disorder with medical and psychological features. He did not meet full criteria for major depressive disorder but was nevertheless thought to require intervention for his mood.
He was treated with twice-daily physical reconditioning. Therapists noted moderate-marked reductions in extremity as well as spinal range of motion, and he was generally deconditioned. He was begun on nortriptyline and titrated to 100 mg/d. Cognitive psychotherapy, biofeedback training, and group psychotherapy were provided. In the course of this, he revealed that 3 years ago his manager had been replaced by a younger man who was abrupt and dismissive, tended to ignore his opinions, and seemed to hold the patient accountable for producing outcomes that had not been specified in advance. The patient had had several discussions with his new boss to no avail and had become increasingly disheartened and frustrated by his work.
His wife was provided counseling in behavioral strategies directed at replacing the role of caretaker with that of wife, which she was relieved to hear.
He and his wife were provided explanations for his pain and information regarding the benign nature of his back condition.
Metabolic consultation was obtained, and he elected to begin a program of diet and exercise, with intent to consider bariatric surgery if results were unsatisfactory in 6 months.
Over the course of several weeks, his pain dropped from typical 7/10 to 4/10, his mood normalized, and his function improved to nearly normal. He resumed socialization, golf, and sexual activity. Sleep normalized.
In several sessions with a vocational counselor, he came to a decision to transfer to a different section in his company. He also negotiated for a desk that could be raised and lowered to permit work standing when he needed to change positions.
REFERENCES
1.Martin BI, Deyo RA, Mirza SK, et al. Expenditures and health status among adults with back and neck problems. JAMA 2008;299(6):656–664.
2.Yu W, Ravelo A, Wagner TH, et al. Prevalence and costs of chronic conditions in the VA health care system. Med Care Res Rev 2003;60 (3 Suppl):146S–167S.
3.Freburger JK, Holmes GM, Agans RP, et al. The rising prevalence of chronic low back pain. Arch Intern Med 2009;169(3):251–258.
4.Gatchel RJ, Polatin PB, Mayer TG, et al. Psychopathology and the rehabilitation of patients with chronic low back pain disability. Arch Phys Med Rehabil 1994;75:666–670.
5.Bigos SJ, Battie MC, Spengler DM, et al. A prospective study of work perceptions and psycho-social factors affecting the report of back injury. Spine 1991;16(1):1–6.
6.Papageorgiou AC, Macfarlane GJ, Thomas E, et al. Psychosocial factors in the workplace—Do they predict new episodes of low back pain? Evidence from the South Manchester Back Pain Study. Spine1997;22(10):1137–1142.
7.Eisenberger NI, Lieberman MD, Williams KD. Does rejection hurt? An FMRI study of social exclusion. Science 2003;302(5643):290–292.
8.Eisenberger NI, Jarcho JM, Lieberman MD, et al. An experimental study of shared sensitivity to physical pain and social rejection. Pain 2006;126(1–3):132–138.
9.Birket-Smith M. Somatization and chronic pain. Acta Anaesthesiol Scand 2001;45:1114–1120.
10.Covington EC. Psychogenic pain: what it means, why it doesn’t exist, and how to diagnose it. Pain Med 2000;1(4):287–294.
11.Xu Q, Yaksh TL. A brief comparison of the pathophysiology of inflammatory versus neuropathic pain. Curr Opin Anaesthesiol 2011;24(4):400–407.
12.Latremoliere A, Woolf CJ. Central sensitization: a generator of pain hypersensitivity by central neural plasticity. J Pain 2009;10(9):895–926.
13.Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain 2011;152:S2–S15.
14.Coghill RC, McHaffie JG, Yen YF. Neural correlates of interindividual differences in the subjective experience of pain. Proc Natl Acad Sci U S A 2003;100(14):8538–8542.
15.Ziv-Sefer S, Raber P, Barbash S, et al. Unity vs. diversity of neuropathic pain mechanisms: allodynia and hyperalgesia in rats selected for heritable predisposition to spontaneous pain. Pain 2009;146(1-2):148–157.
16.Lötsch J, Geisslinger G. Current evidence for a modulation of nociception by human genetic polymorphisms. Pain 2007;132(1-2):18–22.
17.Berna C, Leknes S, Holmes EA, et al. Induction of depressed mood disrupts emotion regulation neurocircuitry and enhances pain unpleasantness. Biol Psychiatry 2010;67(11):1083–1090.
18.Zelman DC, Howland EW, Nichols SN, et al. The effects of induced mood on laboratory pain. Pain 1991;46:105–111.
19.Rainville P, Bao QVH, Chrétien P. Pain-related emotions modulate experimental pain perception and autonomic responses. Pain 2005;118 (3):306–318.
20.Bair MJ, Robinson RL, Katon W, et al. Depression and pain comorbidity: a literature review. Arch Intern Med 2003;163:2433–2445.
21.Bair MJ, Wu J, Damush TM, et al. Association of depression and anxiety alone and in combination with chronic musculoskeletal pain in primary care patients. Psychosom Med2008;70(8):890–897.
22.Miller LR, Cano A. Comorbid chronic pain and depression: who is at risk? J Pain 2009;10(6):619–627.
23.Ohayon MM, Schatzberg AF. Using chronic pain to predict depressive morbidity in the general population. Arch Gen Psychiatry 2003;60(1):39–47.
24.Rudy T, Kerns RD, Turk DC. Chronic pain and depression: toward a cognitive-behavioral mediation model. Pain 1988;35:129–140.
25.McWilliams LA, Goodwin RD, Cox BJ. Depression and anxiety associated with three pain conditions: results from a nationally representative sample. Pain 2004;111(1-2):77–83.
26.Gerhardt A, Mechthild H, Schuller-Roma B, et al. The prevalence and type of axis-I and axis-II mental disorders in subjects with nonspecific chronic back pain: results from a population-based study. Pain Med 2011;12:1231–1240.
27.Edwards RR, Klick B, Buenaver L, et al. Symptoms of distress as prospective predictors of pain-related sciatica treatment outcomes. Pain 2007;130(1-2):47–55.
28.Shipherd JC, Keyes M, Jovanovic T, et al. Veterans seeking treatment for posttraumatic stress disorder: what about comorbid chronic pain? J Rehabil Res Dev 2007;44(2):153–166.
29.Beck JG, Clapp JD. A different kind of co-morbidity: understanding posttraumatic stress disorder and chronic pain. Psychol Trauma 2011;3(2):101–108.
30.Defrin R, Ginzburg K, Solomon Z, et al. Quantitative testing of pain perception in subjects with PTSD—implications for the mechanism of the coexistence between PTSD and chronic pain. Pain2008;138(2):450–459.
31.Knaster P, Karlsson H, Estlander AM, et al. Psychiatric disorders as assessed with SCID in chronic pain patients: the anxiety disorders precede the onset of pain. Gen Hosp Psychiatry2012;34(1):46–52.
32.Stewart SH, Asmundson GJ. Anxiety sensitivity and its impact on pain experiences and conditions: a state of the art. Cogn Behav Ther 2006;35(4):185–188.
33.Thompson T, Keogh E, French CC, et al. Anxiety sensitivity and pain: generalisability across noxious stimuli. Pain 2008;134(1-2):187–196.
34.Gureje O, Simon GE, Von Kor M. A cross-national study of the course of persistent pain in primary care. Pain 2001;92:195–200.
35.Williams LS, Jones WJ, Shen J, et al. Outcomes of newly referred neurology outpatients with depression and pain. Neurology 2004;63 (4):674–677.
36.Kroenke K, Shen J, Oxman TE, et al. Impact of pain on the outcomes of depression treatment: results from the RESPECT trial. Pain 2008;134(1-2):209–215.
37.Shaw WS, Means-Christensen AJ, Slater MA, et al. Psychiatric disorders and risk of transition to chronicity in men with first onset low back pain. Pain Med 2010;11(9):1391–1400.
38.Wylde V, Hewlett S, Learmonth ID, et al. Persistent pain after joint replacement: prevalence, sensory qualities and post-operative determinants. Pain 2011;152:566–572.
39.Maletic V, Raison CL. Neurobiology of depression, fibromyalgia and neuropathic pain. Front Biosci 2009;14:5291–5338.
40.Kim H, Chen L, Lim G, et al. Brain indoleamine 2,3-dioxygenase contributes to the comorbidity of pain and depression. J Clin Invest 2012;122(8):2940–2954.
41.Fishbain DA, Lewis JE, Bruns D, et al. Exploration of anger constructs in acute and chronic pain patients vs. community patients. Pain Pract 2011;11(3):240–251.
42.Trost Z, Vangronsveld K, Linton SJ, et al. Cognitive dimensions of anger in chronic pain. Pain 2012;153(3):515–517.
43.Fernandez E, Turk DC. The scope and significance of anger in the experience of chronic pain. Pain 1995;61(2):165–175.
44.Kerns RD, Rosenberg R, Jacob MC. Anger expression and chronic pain. J Behav Med 1994;17(1):57–67.
45.Carson JW, Keefe FJ, Goli V, et al. Forgiveness and chronic low back pain: a preliminary study examining the relationship of forgiveness to pain, anger, and psychological distress. J Pain 2005;6(2):84–91.
46.Wood AM, Froh JJ, Geraghty AW. Gratitude and well-being: a review and theoretical integration. Clin Psychol Rev 2010;30(7):890–905.
47.Fernando GA. Bloodied but unbowed: resilience examined in a South Asian community. Am J Orthopsychiatry 2012;82(3):367–375.
48.Froh JJ, Yurkewicz C, Kashdan TB. Gratitude and subjective well-being in early adolescence: examining gender differences. J Adolesc 2009;32(3):633–650.
49.Ng MY, Wong WS. The differential effects of gratitude and sleep on psychological distress in patients with chronic pain. J Health Psychol 2013;18(2):263–271.
50.Legrain V, Damme SV, Eccleston C. A neurocognitive model of attention to pain: behavioral and neuroimaging evidence. Pain 2009;144(3):230–232.
51.Fields HL, Malick A, Burstein R. Dorsal horn projection targets of ON and OFF cells in the rostral ventromedial medulla. J Neurophysiol 1995;74(4):1742–1759.
52.Neugebauer V, Li W, Bird GC, et al. The amygdala and persistent pain. Neuroscientist 2004;10(3):221–234.
53.Bushnell MC, Duncan GH, Hofbauer RK, et al. Pain perception: is there a role for primary somatosensory cortex? Proc Natl Acad Sci U S A 1999;96(14):7705–7709.
54.Sprenger C, Eippert F, Finsterbusch J, et al. Attention modulates spinal cord responses to pain. Curr Biol 2012;22(11):1019–1022.
55.Petrovic P, Petersson KM, Ghatan PH, et al. Pain-related cerebral activation is altered by a distracting cognitive task. Pain 2000;85:19–30.
56.Iles RA, Davidson M, Taylor NF, et al. Systematic review of the ability of recovery expectations to predict outcomes in non-chronic non-specific low back pain. J Occup Rehabil2009;19(1):25–40.
57.Clay FJ, Newstead SV, Watson WL, et al. Bio-psychosocial determinants of persistent pain 6 months after non-life-threatening acute orthopaedic trauma. J Pain 2010;11(5):420–430.
58.Kalauokalani D, Cherkin DC, Sherman KJ, et al. Lessons from a trial of acupuncture and massage for low back pain: patient expectations and treatment effects. Spine (Phila Pa 1976)2001;26(13):1418–1424.
59.Koyama T, McHaffie JG, Laurientit PJ, et al. The subjective experience of pain: where expectations become reality. Proc Natl Acad Sci U S A 2005;102(36):12950–12955.
60.Sawamoto N, Honda M, Okada T, et al. Expectation of pain enhances responses to nonpainful somatosensory stimulation in the anterior cingulate cortex and parietal operculum/posterior insula: an event-related functional magnetic resonance imaging study. J Neurosci 2000;20(19):7438–7445.
61.Vlaeyen JWS, Linton SJ. Fear-avoidance and its consequences in chronic musculoskeletal pain: a state of the art. Pain 2000;85:317–332.
62.Vlaeyen JW, Linton SJ. Fear-avoidance model of chronic musculoskeletal pain: 12 years on. Pain 2012;153(6):1144–1147.
63.Kori SH, Miller RP, Todd DD. Kinesiophobia: a new view of chronic pain behavior. Pain Manag 1990;3(1):35–43.
64.McCracken LM, Spertus IL, Janeck AS, et al. Behavioral dimensions of adjustment in persons with chronic pain: pain-related anxiety and acceptance. Pain 1999;80:283–289.
65.Crombex G, Vlaeyen JWS, Heuts PHTG, et al. Pain-related fear is more disabling than pain itself: evidence on the role of pain-related fear in chronic back pain disability. Pain1999;80:329–339.
66.Crombez G, Van Damme S, Eccleston C. Hypervigilance to pain: an experimental and clinical analysis. Pain 2005;116(1-2):4–7.
67.Vlaeyen JW, Linton SJ. Are we “fear-avoidant”? Pain 2006;124(3):240–241.
68.Beck AT, Rush AJ, Shaw BF, Emery G. Cognitive therapy of depression. New York, NY: The Guilford Press, 1979.
69.Turk DC, Meichenbaum D, Genest M. Pain and behavioral medicine: a cognitive-behavioral perspective. New York, NY: Guilford Press, 1983.
70.Turk DC, Rudy TE. Assessment of cognitive factors in chronic pain: a worthwhile enterprise? J Consult Clin Psychol 1986;54(6):760–768.
71.Jensen MP, Turner JA, Romano JM, et al. Coping with chronic pain: a critical review of the literature. Pain 1991;47:249–283.
72.Affleck G, Urrows S, Tennen H, et al. Daily coping with pain from rheumatoid arthritis: patterns and correlates. Pain 1992;51:221–229.
73.Melzack R. Neurophysiology of pain. In: Sternbach RA, ed. The psychology of pain, 2nd ed. New York, NY: Raven Press, 1986.
74.Ahles TA, Blanchard EB, Ruckdeschel JC. The multidimensional nature of cancer-related pain. Pain 1983;17:277–288.
75.Weissman-Fogel I, Sprecher E, Pud D. Effects of catastrophizing on pain perception and pain modulation. Exp Brain Res 2008;186(1):79–85.
76.Turk DC, Rudy TE. Cognitive factors and persistent pain: a glimpse into Pandora’s box. Cogn Ther Res 1992;16(2):99–122.
77.Keefe FJ, Brown GK, Wallston KA, et al. Coping with rheumatoid arthritis pain: catastrophizing as a maladaptive strategy. Pain 1989;37:51–56.
78.Jensen MP, Moore MR, Bockow TB, et al. Psychosocial factors and adjustment to chronic pain in persons with physical disabilities: a systematic review. Arch Phys Med Rehabil2011;92(1):146–160.
79.Ciccone DS, Grzesiak RC. Cognitive dimensions of chronic pain. Soc Sci Med 1984;19(12):1339–1345.
80.Seligman ME. Learned helplessness. Annu Rev Med 1972;23:407–412.
81.Bandura A. Self-efficacy: toward a unifying theory of behavioral change. Psychol Rev 1977;84:191–215.
82.Jensen MP, Turner JA, Romano JM. Self-efficacy and outcome expectancies: relationship to chronic pain coping strategies and adjustment. Pain 1991;44:263–269.
83.Maly MR, Costigan PA, Olney SJ. Self-efficacy mediates walking performance in older adults with knee osteoarthritis. J Gerontol A Biol Sci Med Sci 2007;62(10):1142–1146.
84.Buckelew SP, Huyser B, Hewett J, et al. Self-efficacy predicting outcome among fibromyalgia subjects. Arthritis Care Res 1996;9(2):97–104.
85.Costa Lda C, Maher CG, McAuley JH, et al. Self-efficacy is more important than fear of movement in mediating the relationship between pain and disability in chronic low back pain. Eur J Pain2011;15(2):213–219.
86.Harkapaa K, Jarvikoski A, Mellin G, et al. Health locus of control beliefs and psychological distress as predictors for treatment outcome in low-back pain patients: results of a 3-month follow-up of a controlled intervention study. Pain 1991;46:35–41.
87.Crisson JE, Keefe FJ. The relationship of locus of control to pain coping strategies and psychological distress in chronic pain patients. Pain 1988;35:147–154.
88.Hadjistavropoulos H, Shymkiw J. Predicting readiness to self-manage pain. Clin J Pain 2007;23(3):259–266.
89.Richard S, Dionne CE, Nouwen A. Self-efficacy and health locus of control: relationship to occupational disability among workers with back pain. J Occup Rehabil 2011;21(3):421–430.
90.Oliveira TH, Oliveira VC, Melo RC, et al. Patients in treatment for chronic low back pain have higher externalised beliefs: a cross-sectional study. Rev Bras Fisioter 2012;16(1):35–39.
91.DeGood DE, Kiernan B. Perception of fault in patients with chronic pain. Pain 1996;64(1):153–159.
92.Delahunty DL, Herberman HB, Craig KJ, et al. Acute and Chronic distress and posttraumatic stress disorder as a function of responsibility for serious motor vehicle accidents. J Consult Clin Psychol1997;65:560–567.
93.Hickling EJ, Blanchard EB, Buckley TC, et al. Effects of attribution of responsibility for motor vehicle accidents on severity of PTSD symptoms, ways of coping, and recovery over six months. J Trauma Stress 1999;12:345–353.
94.Hart T, Hanks R, Bogner J, et al. Blame attribution in intentional and unintentional traumatic brain injury: longitudinal changes and impact on subjective well-being. Rehabil Psychol2007;52: 152–161.
95.Hamilton JC, Eger M, Razzak S, et al. Somatoform, factitious, and related diagnoses in the national hospital discharge survey: addressing the proposed DSM-5 revision. Psychosomatics2013;54(2):142.
96.Dimsdale J, Creed F. DSM-5 Workgroup on Somatic Symptom Disorders. The proposed diagnosis of somatic symptom disorders in DSM-5 to replace somatoform disorders in DSM-IV—a preliminary report. J Psychosom Res 2009;66(6):473–476.
97.World Health Organization. The ICD-10 classification of mental and behavioural disorders. Clinical descriptions and diagnostic guidelines. Geneva, Switzerland: WHO, 1992.
98.American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th Text Revision ed. Washington, DC: American Psychiatric Association, 2000.
99.American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 5th ed. Arlington, VA: American Psychiatric Association, 2013.
100.van der Kolk BA, Pelcovitz D, Roth S, et al. Dissociation, somatization, and affect dysregulation: the complexity of adaptation of trauma. Am J Psychiatry 1996;153(7 Suppl):83–93.
101.U.S. Commission on the Evaluation of Pain. Report of the Commission on the Evaluation of Pain, Appendix C: Summary of the National Study of Chronic Pain Syndrome. Washington, DC: Social Security Administration, Office of Disability, 1987.
102.Mailis-Gagnon A, Nicholson K, Blumberger D, et al. Characteristics and period prevalence of self-induced disorder in patients referred to a pain clinic with the diagnosis of complex regional pain syndrome. Clin J Pain 2008;24(2):176–185.
103.Fishbain DA, Cutler R, Rosomoff HL, et al. Chronic pain disability exaggeration/malingering and submaximal effort research. Clin J Pain 1999;15(4):244–274.
104.Bytzer P, Stokholm M, Andersen I, et al. Prevalence of surreptitious laxative abuse in patients with diarrhea of uncertain origin: a cost benefit analysis of a screening procedure. Gut1989;30(10):1379–1384.
105.Rickards FW, De Vidi S. Exaggerated hearing loss in noise induced hearing loss compensation claims in Victoria. Med J Aust 1995;163(7):360–363.
106.Schmand B, Lindeboom J, Schagen S, et al. Cognitive complaints in patients after whiplash injury: the impact of malingering. J Neurol Neurosurg Psychiatry 1998;64(3):339–343.
107.Gervais RO, Russell AS, Green P, et al. Effort testing in patients with fibromyalgia and disability incentives. J Rheumatol 2001;28(8):1892–1899.
108.Rivat C, Becker C, Blugeot A, et al. Chronic stress induces transient spinal neuroinflammation, triggering sensory hypersensitivity and long-lasting anxiety-induced hyperalgesia. Pain2010;150(2):358–368.
109.Le Roy C, Laboureyras E, Gavello-Baudy S, et al. Endogenous opioids released during non-nociceptive environmental stress induce latent pain sensitization via a NMDA-dependent process. J Pain2011;12(10):1069–1079.
110.Green PG, Alvarez P, Gear RW, et al. Further validation of a model of fibromyalgia syndrome in the rat. J Pain 2011;12(7):811–818.
111.Kuzma J, Black D. Chronic widespread pain and psychiatric disorders in veterans of the first Gulf War. Curr Pain Headache Rep 2006;10(2):85–89.
112.Ginzburg K, Solomon Z. Trajectories of stress reactions and somatization symptoms among war veterans: a 20-year longitudinal study. Psychol Med 2011;41(2):353–362.
113.Fordyce WE, Fowler RS, Lehman F, et al. Operant conditioning in the treatment of chronic pain. Arch Phys Med Rehabil 1973;54(9):399–408.
114.Fordyce WE. Behavioral methods for chronic pain and illness. St. Louis, MO: C.V. Mosby, 1976.
115.Fishbain DA, Rosomoff HL, Cutler RB, et al. Secondary gain concept: a review of the scientific evidence. Clin J Pain 1995;11:6–21.
116.Rohling ML, Binder LM, Langhinrichsen-Rohling J. Money matters: a meta-analytic review of the association between financial compensation and the experience and treatment of chronic pain. Health Psychol 1995;14(6):537–547.
117.Hasenbring M, Marienfeld G, Kuhlendahl D, et al. Risk factors of chronicity in lumbar disc patients. A prospective investigation of biologic, psychologic, and social predictors of therapy outcome. Spine1994;19(24):2759–2765.
118.Nguyen TH, Randolph DC, Talmage J, et al. Long-term outcomes of lumbar fusion among workers’ compensation subjects: a historical cohort study. Spine 2011;36(4):320–331.
119.Pence LB, Thorn BE, Jensen MP, et al. Examination of perceived spouse responses to patient well and pain behavior in patients with headache. Clin J Pain 2008;24(8):654–661.
120.Alschuler KN, Hoodin F, Murphy SL, et al. Factors contributing to physical activity in a chronic low back pain clinical sample: a comprehensive analysis using continuous ambulatory monitoring. Pain2011;152(11):2521–2527.
121.Raichle KA, Romano JM, Jensen MP. Partner responses to patient pain and well behaviors and their relationship to patient pain behavior, functioning, and depression. Pain2011;152(1):82–88.
122.Flor H. The functional organization of the brain in chronic pain. In: Sandkahler B, Bromm GF Gebhart, eds. Progress in brain research, Vol. 129. Elsevier Science B.V., 2000:315.
123.Hölzl R, Kleinböhl D, Huse E. Implicit operant learning of pain sensitization. Pain 2005;115(1-2):12–20.
124.Spearing NM, Connelly LB, Nghiem HS, et al. Research on injury compensation and health outcomes: ignoring the problem of reverse causality led to a biased conclusion. J Clin Epidemiol2012;65(11):1219–1226.
125.Spearing NM, Connelly LB, Gargett S, et al. Does injury compensation lead to worse health after whiplash? A systematic review. Pain 2012;153(6):1274–1282.
126.Hagekull B, Bohlin G. Predictors of middle childhood psychosomatic problems: an emotion regulation approach. Infant Child Dev 2004;13:389–405.
127.Payne B, Norfleet MA. Chronic pain and the family: a review. Pain 1986;26:1–22.
128.Roy R. Marital and family issues in patients with chronic pain: a review. Psychother Psychosom 1982;37:1–12.
129.Roy R. Pain-prone patient: a revisit. Psychother Psychosom 1982;37:202–213.
130.Bendixen M, Muus KM, Schei B. The impact of child sexual abuse—A study of a random sample of Norwegian students. Child Abuse Negl 1994;18(10):837–847.
131.Walsh CA, Jamieson E, Macmillan H, et al. Child abuse and chronic pain in a community survey of women. J Interpers Violence 2007;22(12):1536–1554.
132.Imbierowicz K, Egle UT. Childhood adversities in patients with fibromyalgia and somatoform pain disorder. Eur J Pain 2003;7(2):113–119.
133.Mallouh SK, Abbey SE, Dillies LA. The role of loss in treatment outcomes of persistent somatization. Gen Hosp Psychiatry 1995;17;187–191.
134.Brown RJ, Schrag A, Trimble MR. Dissociation, childhood interpersonal trauma, and family functioning in patients with somatization disorder. Am J Psychiatry 2005;162:899–905.
135.Sachs-Ericsson N, Kendall-Tackett K, Hernandez A. Childhood abuse, chronic pain, and depression in the National Comorbidity Survey. Child Abuse Negl 2007;31(5):531–547.
136.Landa A, Peterson BS, Fallon BA. Somatoform pain: a developmental theory and translational research review. Psychosom Med 2012;74(7):717–727.
137.Ringel Y, Drossman DA, Leserman JL, et al. Effect of abuse history on pain reports and brain responses to aversive visceral stimulation: an FMRI study. Gastroenterology2008;134(2):396–404.
138.Coutinho SV, Plotsky PM, Sablad M, et al. Neonatal maternal separation alters stress-induced responses to viscerosomatic nociceptive stimuli in rat. Am J Physiol Gastrointest Liver Physiol2002;282(2):G307–G316.
139.Greena PG, Chena X, Alvareza P, et al. Early-life stress produces muscle hyperalgesia and nociceptor sensitization in the adult rat. Pain 2011;152:2549–2556.
140.Porter LS, Davis D, Keefe FJ. Attachment and pain: recent findings and future directions. Pain 2007;128(3):195–198.
141.McWilliams LA, Asmundson GJG. The relationship of adult attachment dimensions to pain-related fear, hypervigilance, and catastrophizing. Pain 2007;127(1-2):27–34.
142.Rome HP, Rome JD. Limbically augmented pain syndrome (LAPS): kindling, corticolimbic sensitization, and the convergence of affective and sensory symptoms in chronic pain disorders. Pain Med2000;1(1):7–23.
143.Arroll B, Goodyear-Smith F, Crengle S, et al. Validation of PHQ-2 and PHQ-9 to screen for major depression in the primary care population. Ann Fam Med 2010;8(4):348–353.
144.Kroenke K, Spitzer RL, Williams JB, et al. Anxiety disorders in primary care: prevalence, impairment, comorbidity, and detection. Ann Intern Med 2007;146(5):317–325.
145.Dworkin SF, Von Korff M, LeResche L. Multiple pains and psychiatric disturbance. An epidemiologic investigation. Arch Gen Psychiatry 1990;47(3):239–244.
146.Streltzer J, Eliashof BA, Kline AE, et al. Chronic pain disorder following physical injury. Psychosomatics 2000;41(3):227–234.
147.Tait RC, Chibnall JT, Krause S: The pain disability index: psychometric properties. Pain 1990;40(2):171–182.
148.Sullivan AB, Scheman J, Venesy D, et al. The role of exercise and types of exercise in the rehabilitation of chronic pain: specific or nonspecific benefits. Curr Pain Headache Rep2012;16(2):153–161.
149.Murtezani A, Hundozi H, Orovcanec N, et al. A comparison of high intensity aerobic exercise and passive modalities for the treatment of workers with chronic low back pain: a randomized, controlled trial. Eur J Phys Rehabil Med 2011;47(3):359–366.
150.De Jong JR, Vlaeyen JWS, Onghena P, et al. Fear of movement/(re) injury in chronic low back pain education or exposure in vivo as mediator to fear reduction? Clin J Pain 2005;21:9–17.
151.Dimeo F, Bauer M, Varahram I, et al. Benefits from aerobic exercise in patients with major depression: a pilot study. Br J Sports Med 2001;35(2):114–117.
152.Herring MP, Puetz TW, O’Connor PJ, et al. Effect of exercise training on depressive symptoms among patients with a chronic illness: a systematic review and meta-analysis of randomized controlled trials. Arch Intern Med 2012;172(2):101–111.
153.Herring MP, Jacob ML, Suveg C, et al. Feasibility of exercise training for the short-term treatment of generalized anxiety disorder: a randomized controlled trial. Psychother Psychosom2012;81(1):21–28.
154.Hayden JA, van Tulder MW, Malmivaara AV, et al. Meta-analysis: exercise therapy for nonspecific low back pain. Ann Intern Med 2005;142(9):765775.
155.Van Tulder MW, Koes BW, Bouter LM. Conservative treatment of acute and chronic nonspecific low back pain. A systematic review of randomized controlled trials of the most common interventions. Spine1997;22(18):2128–2156.
156.Van der Velde G, Mierau D. The effect of exercise on percentile rank aerobic capacity, pain, and self-rated disability in patients with chronic low-back pain: a retrospective chart review. Arch Phys Med Rehabil 2000;81:1457–1463.
157.Ljunggren AE, Weber H, Kogstad O, et al. Effect of exercise on sick leave due to low back pain. A randomized, comparative, long-term study. Spine 1997;22(14):1610–1616.
158.Brox JI, Reikeras O, Nygaard O, et al. Lumbar instrumented fusion compared with cognitive intervention and exercises in patients with chronic back pain after previous surgery for disc herniation: a prospective randomized controlled study. Pain 2006;122(1-2):145–155.
159.Cherkin DC, Sherman KJ, Kahn J, et al. A comparison of the effects of 2 types of massage and usual care on chronic low back pain: a randomized, controlled trial. Ann Intern Med2011;155(1):1–9
160.Crane JD, Ogborn DI, Cupido C, et al. Massage therapy attenuates inflammatory signaling after exercise-induced muscle damage. Sci Transl Med 2012;4(119):119ra13.
161.Lewis M, Johnson MI. The clinical effectiveness of therapeutic massage for musculoskeletal pain: a systematic review. Physiotherapy 2006;92(3):146–158.
162.Roth RS, Punch MR, Bachman JE. Patient beliefs about pain diagnosis in chronic pelvic pain: relation to pain experience, mood and disability. J Reprod Med 2011;56(3-4):123–129.
163.Nieto R, Raichle KA, Jensen MP, et al. Changes in pain-related beliefs, coping, and catastrophizing predict changes in pain intensity, pain interference, and psychological functioning in individuals with myotonic muscular dystrophy and facioscapulohumeral dystrophy. Clin J Pain 2012;28(1):47–54.
164.Pons T, Shipton E, Mulder R. The Relationship between beliefs about pain and functioning with rheumatologic conditions. Rehabil Res Pract 2012;2012:206263.
165.Williams DA, Thorn BE. An empirical assessment of pain beliefs. Pain 1989;36:351–358.
166.Waddell G, Newton M, Henderson I, et al. A fear avoidance beliefs questionnaire (FABQ) and the role of fear avoidance beliefs in chronic low back pain and disability. Pain1993;52:157–168.
167.Fernandez E, Turk DC. The utility of cognitive coping strategies for altering pain perception: a meta-analysis. Pain 1989;38:123–135.
168.Compas BE, Haaga DA, Keefe FJ, et al. Sampling of empirically supported psychological treatments from health psychology: smoking, chronic pain, cancer, and bulimia nervosa. J Consult Clin Psychol1998;66(1):89–112.
169.Morley S, Eccleston C, Williams A. Systematic review and meta-analysis of randomized controlled trials of cognitive behavior therapy and behavior therapy for chronic pain in adults, excluding headache. Pain 1999;80:1–13.
170.Glombiewski JA, Sawyer AT, Gutermann J, et al. Psychological treatments for fibromyalgia: a meta-analysis. Pain 2010;151(2): 280–295.
171.Wetering EJ, Lemmens KM, Nieboer AP, et al. Cognitive and behavioral interventions for the management of chronic neuropathic pain in adults—a systematic review. Eur J Pain2010;14(7):670–681.
172.Hoffman BM, Papas RK, Chatkoff DK, et al. Meta-analysis of psychological interventions for chronic low back pain. Health Psychol 2007;26(1):1–9.
173.Herbert B. The relaxation response. New York, NY: William Morrow and Company, Inc., 1975
174.Chang BH, Dusek JA, Benson H. Psychobiological changes from relaxation response elicitation: long-term practitioners vs. novices. Psychosomatics 2011;52(6):550–559.
175.McCracken LM, Carson JW, Eccleston C, et al. Acceptance and change in the context of chronic pain. Pain 2004;109(1-2):4–7.
176.McCracken LM, Gauntlett-Gilbert J, Vowles KE. The role of mindfulness in a contextual cognitive-behavioral analysis of chronic pain-related suffering and disability. Pain 2007;131(1-2):63–69.
177.Potter JS. NIH Pain Consortium 7th Annual NIH Symposium on Advances in n Research. Washington, DC. 2012.
178.Zeidan F, Grant JA, Brown CA, et al. Mindfulness meditation-related pain relief: evidence for unique brain mechanisms in the regulation of pain. Neurosci Lett 2012;520(2):165–173.
179.Baranoff J, Hanrahan SJ, Kapur D, et al. Acceptance as a process variable in relation to catastrophizing in multidisciplinary pain treatment. Eur J Pain 2013;17(1):101–110.
180.Cassidy EL, Atherton RJ, Robertson N, et al. Mindfulness, functioning and catastrophizing after multidisciplinary pain management for chronic low back pain. Pain 2012;153(3):644–650.
181.Prevedini AB, Presti G, Rabitti E, et al. Acceptance and commitment therapy (ACT): the foundation of the therapeutic model and an overview of its contribution to the treatment of patients with chronic physical diseases. G Ital Med Lav Ergon 2011;33(1 Suppl A): A53–A63.
182.Hayes SC, Luoma J, Bond F, et al. Acceptance and commitment therapy: model, processes, and outcomes. Behav Res Ther 2006;44(1):1–25.
183.Wicksell RK, Melin L, Lekander M, et al. Evaluating the effectiveness of exposure and acceptance strategies to improve functioning and quality of life in longstanding pediatric pain—a randomized controlled trial. Pain 2009;141(3):248–257.
184.Veehof MM, Oskam MJ, Schreurs KM, et al. Acceptance-based interventions for the treatment of chronic pain: a systematic review and meta-analysis. Pain 2011;152:533–542.
185.Rosomoff HL, Rosomoff RS. Comprehensive multidisciplinary pain center approach to the treatment of low back pain. Neurosurg Clin N Am 1991;2(4):877–890.
186.National Institutes of Health (NIH), Technology Assessment Panel on Integration of Behavioral and Relaxation Approaches into the Treatment of Chronic Pain and Insomnia. Integration of behavioral and relaxation approaches into the treatment of chronic pain and insomnia. JAMA 1996;276(4):313–338.
187.Karavidas MK, Tsai PS, Yucha C, et al. Thermal biofeedback for primary Raynaud’s phenomenon: a review of the literature. Appl Psychophysiol Biofeedback 2006;31(3):203–216.
188.Rainforth MV, Schneider RH, Nidich SI, et al. Stress reduction programs in patients with elevated blood pressure: a systematic review and meta-analysis. Curr Hypertens Rep2007;9(6):520–528.
189.Bruehl S, Chung OY. Psychological and behavioral aspects of complex regional pain syndrome management. Clin J Pain 2006;22(5):430–437.
190.Babu AS, Mathew E, Danda D, et al. Management of patients with fibromyalgia using biofeedback: a randomized control trial. Indian J Med Sci 2007;61:455–461.
191.Van Tulder MW, Ostelo R, Vlaeyen JW, et al. Behavioral treatment for chronic low back pain: a systematic review within the framework of the Cochrane back review group. Spine2000;25:2688–2699.
192.Gatchel RJ, Stowell AW, Wildenstein L, et al. Efficacy of an early intervention for patients with acute temporomandibular disorder-related pain: a one-year outcome study. J Am Dent Assoc2006;137(3):339–347.
193.Akkaya N, Ardic F, Ozgen M, et al. Efficacy of electromyographic biofeedback and electrical stimulation following arthroscopic partial meniscectomy: a randomized controlled trial. Clin Rehabil2012;26(3):224–236.
194.Chiarioni G, Nardo A, Vantini I, et al. Biofeedback is superior to electrogalvanic stimulation and massage for treatment of levator ani syndrome. Gastroenterology 2010;138:1321–1329.
195.Spence SH, Champion D, Newton-John T, et al. Effect of EMG biofeedback compared to applied relaxation training with chronic, upper extremity cumulative trauma disorders. Pain1995;63(2):199–206.
196.Haefner HK, Collins ME, Davis GD, et al. The vulvodynia guideline. J Low Genit Tract Dis 2005;9(1):40–51.
197.Bergeron S, Binik YM, Khalife S, et al. A randomized comparison of group cognitive-behavioral therapy, surface electromyographic biofeedback, and vestibulectomy in the treatment of dyspareunia resulting from vulvar vestibulitis. Pain 2001;91:297–306.
198.Aggarwal VR, Lovell K, Peters S, et al. Psychosocial interventions for the management of chronic orofacial pain. Cochrane Database Syst Rev 2011;11:CD008456.
199.Sierpina V, Astin J, Giordano J. Mind-body therapies for headache. Am Fam Physician 2007;76(10):1518–1522.
200.Astin JA. Mind–body therapies for the management of pain. Clin J Pain 2004;20(1):27–32.
201.Nestoriuc Y, Martin A. Efficacy of biofeedback for migraine: a meta-analysis. Pain 2007;128;111–127.
202.Andrasik F. Biofeedback in headache: an overview of approaches and evidence. Cleve Clin J Med 2010;77(Suppl 3):S72–S76.
203.Nestoriuc Y, Rief W, Martin A. Meta-analysis of biofeedback for tension-type headache: efficacy, specificity, and treatment moderators. J Consult Clin Psychol 2008;76:379–396.
204.Mullally WJ, Hall K, Goldstein R. Efficacy of biofeedback in the treatment of migraine and tension type headaches. Pain Physician 2009;12(6):1005–1011.
205.Holroyd KA, Cottrell CK, O’Donnell FJ, et al. Effect of preventive (beta blocker) treatment, behavioural migraine management, or their combination on outcomes of optimised acute treatment in frequent migraine: randomised controlled trial. BMJ 2010;341:c4871.
206.Dellve L, Ahlstrom L, Jonsson A, et al. Myofeedback training and intensive muscular strength training to decrease pain and improve work ability among female workers on long-term sick leave with neck pain: a randomized controlled trial. Int Arch Occup Environ Health 2011;84(3):335–346.
207.Ma C, Szeto GP, Yan T, et al. Comparing biofeedback with active exercise and passive treatment for the management of work-related neck and shoulder pain: a randomized controlled trial. Arch Phys Med Rehabil 2011;92(6):849–858.
208.Ehrenborg C, Archenholtz B. Is surface EMG biofeedback an effective training method for persons with neck and shoulder complaints after whiplash-associated disorders concerning activities of daily living and pain—a randomized controlled trial. Clin Rehabil 2010;24(8):715–726.
209.Neblett R, Mayer TG, Brede E, et al. Correcting abnormal flexion-relaxation in chronic lumbar pain: responsiveness to a new biofeedback training protocol. Clin J Pain 2010;26(5):403–409.
210.Glombiewski JA, Hartwich-Tersek J, Rief W. Two psychological interventions are effective in severely disabled, chronic back pain patients: a randomised controlled trial. Int J Behav Med2010;17(2):97–107.
211.Yang ZS, Zu XB, Qi L, et al. Combination therapy of biofeedback with electrical stimulation for chronic prostatitis/chronic pelvic pain syndrome. Zhonghua Nan Ke Xue 2011;17(7):611–6114.
212.Kayiran S, Dursun E, Ermutlu N, et al. Neurofeedback in fibromyalgia syndrome. Agri 2007;19(3):47–53.
213.Stokes DA, Lappin MS. Neurofeedback and biofeedback with 37 migraineurs: a clinical outcome study. Behav Brain Funct 2010;6:9.
214.Turner JA, Chapman CR. Psychological interventions for chronic pain: a critical review. II. Operant conditioning, hypnosis and cognitive-behavioral therapy. Pain 1982;12:23–46.
215.Sanders SH. Operant therapy with pain patients: evidence for its effectiveness. In: Lebovits AH, ed. Seminars in pain medicine, 1st ed. Philadelphia, PA: W.B. Saunders, 2003:90–98.
216.Thieme K, Flor H, Turk DC. Psychological pain treatment in fibro-myalgia syndrome: efficacy of operant behavioural and cognitive behavioural treatments. Arthritis Res Ther2006;8(4):R121.
217.Lewandowski W, Morris R, Draucker CB, et al. Chronic pain and the family: theory-driven treatment approaches. Issues Ment Health Nurs 2007;28(9):1019–1044.
218.McCracken LM. Social context and acceptance of chronic pain: the role of solicitous and punishing responses. Pain 2005;113:155–159.
219.Flor H, Fydrich T, Turk DC. Efficacy of multidisciplinary pain treatment centers: a meta-analytic review. Pain 1992;49:221–230.
220.Turk DC. Efficacy of multidisciplinary pain centers in the treatment of chronic pain. In: Cohen MJM, Campbell NJ, eds. Pain treatment centers at a crossroads: a practical and conceptual reappraisal, progress in pain research and management, vol. 7. Seattle, WA: IASP Press, 1996:257–273.
221.Tollison CD, Kriegel ML, Downie GR. Chronic low back pain: results of treatment at the Pain Therapy Center. South Med J 1985;78(11):1291–1295.
222.Gatchel RJ, Okifuji A. Evidence-based scientific data documenting the treatment and cost-effectiveness of comprehensive pain programs for chronic nonmalignant pain. J Pain2006;7(11):779–793.
223.Turk DC, Swanson K. Efficacy and cost-effectiveness treatment for chronic pain: an analysis and evidence-based synthesis. In: Schatman ME, Campbell A, eds. Chronic pain management: a guidebook for multidisciplinary program development. New York, NY: Informa Healthcare, 2007:15–38.
224.Darchuk KM, Townsend CO, Rome JD, et al. Longitudinal treatment outcomes for geriatric patients with chronic non-cancer pain at an interdisciplinary pain rehabilitation program. Pain Med2010;11(9):1352–1364.
225.Angst F, Françoise G, Verra M, et al. Interdisciplinary rehabilitation after whiplash injury: an observational prospective outcome study. J Rehabil Med 2010;42(4):350–356.
226.Patterson M, Huffman K, Scheman J, et al. Treatment of complex regional pain syndrome (RSD): a study of outcomes from an interdisciplinary chronic pain rehabilitation program. Pain Med 2011;12(3):497 (meeting abstracts)American Academy of Pain Medicine 27th Annual Meeting, March 24-27, 2011, Washington.
227.Busch H, Bodin L, Bergström G, et al. Patterns of sickness absence a decade after pain-related multidisciplinary rehabilitation. Pain 2011;152:1727–1733.
228.http://www.theacpa.org/. Accessed April 20, 2008.